What happens when you have an allergy ap bio

This animation from Rockefeller University shows how dendritic cells act as sentinels in the bodys immune system.

Lymphocytes in human circulating blood are approximately 80 to 90 percent T cells, shown in Figure , and 10 to 20 percent B cells. Recall that the T cells are involved in the cell-mediated immune response, whereas B cells are part of the humoral immune response.

T cells encompass a heterogeneous population of cells with extremely diverse functions.

Some T cells reply to APCs of the innate immune system, and indirectly induce immune responses by releasing cytokines. Other T cells stimulate B cells to prepare their own response. Another population of T cells detects APC signals and directly kills the infected cells. Other T cells are involved in suppressing inappropriate immune reactions to harmless or “self” antigens.

T and B cells exhibit a common theme of recognition/binding of specific antigens via a complementary receptor, followed by activation and self-amplification/maturation to specifically bind to the specific antigen of the infecting pathogen.

T and B lymphocytes are also similar in that each cell only expresses one type of antigen receptor. Any individual may possess a population of T and B cells that together express a near limitless variety of antigen receptors that are capable of recognizing virtually any infecting pathogen. T and B cells are activated when they recognize little components of antigens, called epitopes, presented by APCs, illustrated in Figure Note that recognition occurs at a specific epitope rather than on the entire antigen; for this reason, epitopes are known as “antigenic determinants.” In the absence of information from APCs, T and B cells remain inactive, or naïve, and are unable to prepare an immune response.

The requirement for information from the APCs of innate immunity to trigger B cell or T cell activation illustrates the essential nature of the innate immune response to the functioning of the entire immune system.

Naïve T cells can express one of two diverse molecules, CD4 or CD8, on their surface, as shown in Figure , and are accordingly classified as CD4+ or CD8+ cells. These molecules are significant because they regulate how a T cell will interact with and reply to an APC.

Naïve CD4+ cells bind APCs via their antigen-embedded MHC II molecules and are stimulated to become helper T (TH) lymphocytes, cells that go on to stimulate B cells (or cytotoxic T cells) directly or secrete cytokines to inform more and various target cells about the pathogenic threat. In contrast, CD8+ cells engage antigen-embedded MHC I molecules on APCs and are stimulated to become cytotoxic T lymphocytes (CTLs), which directly kill infected cells by apoptosis and emit cytokines to amplify the immune response. The two populations of T cells own diverse mechanisms of immune protection, but both bind MHC molecules via their antigen receptors called T cell receptors (TCRs).

The CD4 or CD8 surface molecules differentiate whether the TCR will engage an MHC II or an MHC I molecule. Because they help in binding specificity, the CD4 and CD8 molecules are described as coreceptors.

Which of the following statements about T cells is false?

  • The T cell receptor is found on both CD4+ and CD8+ T cells.
  • Compare and contrast adaptive and innate immunity
  • Describe cell-mediated immune response and humoral immune response
  • MHC II is a receptor found on most body cells, while MHC I is a receptor found on immune cells only.
  • Helper T cells are CD4+, while cytotoxic T cells are CD8+.
  • Explain adaptive immunity
  • Helper T cells release cytokines while cytotoxic T cells kill the infected cell.
  • Describe immune tolerance

Consider the innumerable possible antigens that an individual will be exposed to during a lifetime.

The mammalian adaptive immune system is adept in responding appropriately to each antigen. Mammals own an huge diversity of T cell populations, resulting from the diversity of TCRs. Each TCR consists of two polypeptide chains that span the T cell membrane, as illustrated in Figure ; the chains are linked by a disulfide bridge. Each polypeptide chain is comprised of a constant domain and a variable domain: a domain, in this sense, is a specific region of a protein that may be regulatory or structural. The intracellular domain is involved in intracellular signaling.

A single T cell will express thousands of identical copies of one specific TCR variant on its cell surface. The specificity of the adaptive immune system occurs because it synthesizes millions of diverse T cell populations, each expressing a TCR that differs in its variable domain. This TCR diversity is achieved by the mutation and recombination of genes that encode these receptors in stem cell precursors of T cells. The binding between an antigen-displaying MHC molecule and a complementary TCR “match” indicates that the adaptive immune system needs to activate and produce that specific T cell because its structure is appropriate to recognize and destroy the invading pathogen.

The TH lymphocytes function indirectly to identify potential pathogens for other cells of the immune system.

These cells are significant for extracellular infections, such as those caused by certain bacteria, helminths, and protozoa. TH lymphocytes recognize specific antigens displayed in the MHC II complexes of APCs. There are two major populations of TH cells: TH1 and TH2. TH1 cells secrete cytokines to enhance the activities of macrophages and other T cells. TH1 cells activate the action of cyotoxic T cells, as well as macrophages. TH2 cells stimulate naïve B cells to destroy foreign invaders via antibody secretion. Whether a TH1 or a TH2 immune response develops depends on the specific types of cytokines secreted by cells of the innate immune system, which in turn depends on the nature of the invading pathogen.

The TH1-mediated response involves macrophages and is associated with inflammation.

Recall the frontline defenses of macrophages involved in the innate immune response. Some intracellular bacteria, such as Mycobacterium tuberculosis, own evolved to multiply in macrophages after they own been engulfed. These pathogens evade attempts by macrophages to destroy and digest the pathogen. When M. tuberculosis infection occurs, macrophages can stimulate naïve T cells to become TH1 cells. These stimulated T cells secrete specific cytokines that send feedback to the macrophage to stimulate its digestive capabilities and permit it to destroy the colonizing M.

tuberculosis. In the same manner, TH1-activated macrophages also become better suited to ingest and kill tumor cells. In summary; TH1 responses are directed toward intracellular invaders while TH2 responses are aimed at those that are extracellular.

When stimulated by the TH2 pathway, naïve B cells differentiate into antibody-secreting plasma cells. A plasma cell is an immune cell that secrets antibodies; these cells arise from B cells that were stimulated by antigens. Similar to T cells, naïve B cells initially are coated in thousands of B cell receptors (BCRs), which are membrane-bound forms of Ig (immunoglobulin, or an antibody).

The B cell receptor has two heavy chains and two light chains connected by disulfide linkages. Each chain has a constant and a variable region; the latter is involved in antigen binding. Two other membrane proteins, Ig alpha and Ig beta, are involved in signaling. The receptors of any specific B cell, as shown in Figure are every the same, but the hundreds of millions of diverse B cells in an individual own distinct recognition domains that contribute to extensive diversity in the types of molecular structures to which they can bind. In this state, B cells function as APCs.

They bind and engulf foreign antigens via their BCRs and then display processed antigens in the context of MHC II molecules to TH2 cells. When a TH2 cell detects that a B cell is bound to a relevant antigen, it secretes specific cytokines that induce the B cell to proliferate rapidly, which makes thousands of identical (clonal) copies of it, and then it synthesizes and secretes antibodies with the same antigen recognition pattern as the BCRs. The activation of B cells corresponding to one specific BCR variant and the dramatic proliferation of that variant is known as clonal selection.

This phenomenon drastically, but briefly, changes the proportions of BCR variants expressed by the immune system, and shifts the balance toward BCRs specific to the infecting pathogen.

T and B cells differ in one fundamental way: whereas T cells bind antigens that own been digested and embedded in MHC molecules by APCs, B cells function as APCs that bind intact antigens that own not been processed. Although T and B cells both react with molecules that are termed “antigens,” these lymphocytes actually reply to extremely diverse types of molecules. B cells must be capable to bind intact antigens because they secrete antibodies that must recognize the pathogen directly, rather than digested remnants of the pathogen.

Bacterial carbohydrate and lipid molecules can activate B cells independently from the T cells.

CTLs, a subclass of T cells, function to clear infections directly. The cell-mediated part of the adaptive immune system consists of CTLs that attack and destroy infected cells. CTLs are particularly significant in protecting against viral infections; this is because viruses replicate within cells where they are shielded from extracellular contact with circulating antibodies. When APCs phagocytize pathogens and present MHC I-embedded antigens to naïve CD8+ T cells that express complementary TCRs, the CD8+ T cells become activated to proliferate according to clonal selection.

These resulting CTLs then identify non-APCs displaying the same MHC I-embedded antigens (for example, viral proteins)—for example, the CTLs identify infected host cells.

Intracellularly, infected cells typically die after the infecting pathogen replicates to a sufficient concentration and lyses the cell, as numerous viruses do. CTLs attempt to identify and destroy infected cells before the pathogen can replicate and escape, thereby halting the progression of intracellular infections. CTLs also support NK lymphocytes to destroy early cancers.

Cytokines secreted by the TH1 response that stimulates macrophages also stimulate CTLs and enhance their ability to identify and destroy infected cells and tumors.

CTLs sense MHC I-embedded antigens by directly interacting with infected cells via their TCRs. Binding of TCRs with antigens activates CTLs to release perforin and granzyme, degradative enzymes that will induce apoptosis of the infected cell.

Recall that this is a similar destruction mechanism to that used by NK cells. In this process, the CTL does not become infected and is not harmed by the secretion of perforin and granzymes. In fact, the functions of NK cells and CTLs are complementary and maximize the removal of infected cells, as illustrated in Figure If the NK cell cannot identify the “missing self” pattern of down-regulated MHC I molecules, then the CTL can identify it by the complicated of MHC I with foreign antigens, which signals “altered self.” Similarly, if the CTL cannot detect antigen-embedded MHC I because the receptors are depleted from the cell surface, NK cells will destroy the cell instead.

CTLs also emit cytokines, such as interferons, that alter surface protein expression in other infected cells, such that the infected cells can be easily identified and destroyed. Moreover, these interferons can also prevent virally infected cells from releasing virus particles.

Based on what you know about MHC receptors, why do you ponder an organ transplanted from an incompatible donor to a recipient will be rejected?

Plasma cells and CTLs are collectively called effector cells: they represent differentiated versions of their naïve counterparts, and they are involved in bringing about the immune defense of killing pathogens and infected host cells.

Learning Objectives

By the finish of this section, you will be capable to:

  1. Compare and contrast adaptive and innate immunity
  2. Describe cell-mediated immune response and humoral immune response
  3. Explain adaptive immunity
  4. Describe immune tolerance

The innate and adaptive immune responses discussed thus far comprise the systemic immune system (affecting the whole body), which is distinct from the mucosal immune system.

Mucosal immunity is formed by mucosa-associated lymphoid tissue, which functions independently of the systemic immune system, and which has its own innate and adaptive components. Mucosa-associated lymphoid tissue (MALT), illustrated in Figure , is a collection of lymphatic tissue that combines with epithelial tissue lining the mucosa throughout the body. This tissue functions as the immune barrier and response in areas of the body with direct contact to the external environment. The systemic and mucosal immune systems use numerous of the same cell types.

Foreign particles that make their way to MALT are taken up by absorptive epithelial cells called M cells and delivered to APCs located directly under the mucosal tissue. M cells function in the transport described, and are located in the Peyer’s patch, a lymphoid nodule. APCs of the mucosal immune system are primarily dendritic cells, with B cells and macrophages having minor roles. Processed antigens displayed on APCs are detected by T cells in the MALT and at various mucosal induction sites, such as the tonsils, adenoids, appendix, or the mesenteric lymph nodes of the intestine. Activated T cells then migrate through the lymphatic system and into the circulatory system to mucosal sites of infection.

MALT is a crucial component of a functional immune system because mucosal surfaces, such as the nasal passages, are the first tissues onto which inhaled or ingested pathogens are deposited.

The mucosal tissue includes the mouth, pharynx, and esophagus, and the gastrointestinal, respiratory, and urogenital tracts.

The immune system has to be regulated to prevent wasteful, unnecessary responses to harmless substances, and more importantly so that it does not attack “self.” The acquired ability to prevent an unnecessary or harmful immune response to a detected foreign substance known not to cause disease is described as immune tolerance. Immune tolerance is crucial for maintaining mucosal homeostasis given the tremendous number of foreign substances (such as food proteins) that APCs of the oral cavity, pharynx, and gastrointestinal mucosa encounter.

Immune tolerance is brought about by specialized APCs in the liver, lymph nodes, little intestine, and lung that present harmless antigens to an exceptionally diverse population of regulatory T (Treg) cells, specialized lymphocytes that suppress local inflammation and inhibit the secretion of stimulatory immune factors. The combined result of Treg cells is to prevent immunologic activation and inflammation in undesired tissue compartments and to permit the immune system to focus on pathogens instead.

In addition to promoting immune tolerance of harmless antigens, other subsets of Treg cells are involved in the prevention of the autoimmune response, which is an inappropriate immune response to host cells or self-antigens. Another Treg class suppresses immune responses to harmful pathogens after the infection has cleared to minimize host cell damage induced by inflammation and cell lysis.

Consider the innumerable possible antigens that an individual will be exposed to during a lifetime.

The mammalian adaptive immune system is adept in responding appropriately to each antigen. Mammals own an huge diversity of T cell populations, resulting from the diversity of TCRs. Each TCR consists of two polypeptide chains that span the T cell membrane, as illustrated in Figure ; the chains are linked by a disulfide bridge. Each polypeptide chain is comprised of a constant domain and a variable domain: a domain, in this sense, is a specific region of a protein that may be regulatory or structural. The intracellular domain is involved in intracellular signaling. A single T cell will express thousands of identical copies of one specific TCR variant on its cell surface.

The specificity of the adaptive immune system occurs because it synthesizes millions of diverse T cell populations, each expressing a TCR that differs in its variable domain. This TCR diversity is achieved by the mutation and recombination of genes that encode these receptors in stem cell precursors of T cells. The binding between an antigen-displaying MHC molecule and a complementary TCR “match” indicates that the adaptive immune system needs to activate and produce that specific T cell because its structure is appropriate to recognize and destroy the invading pathogen.

The TH lymphocytes function indirectly to identify potential pathogens for other cells of the immune system.

These cells are significant for extracellular infections, such as those caused by certain bacteria, helminths, and protozoa. TH lymphocytes recognize specific antigens displayed in the MHC II complexes of APCs. There are two major populations of TH cells: TH1 and TH2. TH1 cells secrete cytokines to enhance the activities of macrophages and other T cells. TH1 cells activate the action of cyotoxic T cells, as well as macrophages.

TH2 cells stimulate naïve B cells to destroy foreign invaders via antibody secretion. Whether a TH1 or a TH2 immune response develops depends on the specific types of cytokines secreted by cells of the innate immune system, which in turn depends on the nature of the invading pathogen.

The TH1-mediated response involves macrophages and is associated with inflammation. Recall the frontline defenses of macrophages involved in the innate immune response. Some intracellular bacteria, such as Mycobacterium tuberculosis, own evolved to multiply in macrophages after they own been engulfed.

These pathogens evade attempts by macrophages to destroy and digest the pathogen. When M. tuberculosis infection occurs, macrophages can stimulate naïve T cells to become TH1 cells. These stimulated T cells secrete specific cytokines that send feedback to the macrophage to stimulate its digestive capabilities and permit it to destroy the colonizing M. tuberculosis. In the same manner, TH1-activated macrophages also become better suited to ingest and kill tumor cells. In summary; TH1 responses are directed toward intracellular invaders while TH2 responses are aimed at those that are extracellular.

When stimulated by the TH2 pathway, naïve B cells differentiate into antibody-secreting plasma cells.

A plasma cell is an immune cell that secrets antibodies; these cells arise from B cells that were stimulated by antigens. Similar to T cells, naïve B cells initially are coated in thousands of B cell receptors (BCRs), which are membrane-bound forms of Ig (immunoglobulin, or an antibody). The B cell receptor has two heavy chains and two light chains connected by disulfide linkages. Each chain has a constant and a variable region; the latter is involved in antigen binding. Two other membrane proteins, Ig alpha and Ig beta, are involved in signaling. The receptors of any specific B cell, as shown in Figure are every the same, but the hundreds of millions of diverse B cells in an individual own distinct recognition domains that contribute to extensive diversity in the types of molecular structures to which they can bind.

In this state, B cells function as APCs. They bind and engulf foreign antigens via their BCRs and then display processed antigens in the context of MHC II molecules to TH2 cells. When a TH2 cell detects that a B cell is bound to a relevant antigen, it secretes specific cytokines that induce the B cell to proliferate rapidly, which makes thousands of identical (clonal) copies of it, and then it synthesizes and secretes antibodies with the same antigen recognition pattern as the BCRs.

The activation of B cells corresponding to one specific BCR variant and the dramatic proliferation of that variant is known as clonal selection. This phenomenon drastically, but briefly, changes the proportions of BCR variants expressed by the immune system, and shifts the balance toward BCRs specific to the infecting pathogen.

T and B cells differ in one fundamental way: whereas T cells bind antigens that own been digested and embedded in MHC molecules by APCs, B cells function as APCs that bind intact antigens that own not been processed.

Although T and B cells both react with molecules that are termed “antigens,” these lymphocytes actually reply to extremely diverse types of molecules. B cells must be capable to bind intact antigens because they secrete antibodies that must recognize the pathogen directly, rather than digested remnants of the pathogen. Bacterial carbohydrate and lipid molecules can activate B cells independently from the T cells.

CTLs, a subclass of T cells, function to clear infections directly.

The cell-mediated part of the adaptive immune system consists of CTLs that attack and destroy infected cells. CTLs are particularly significant in protecting against viral infections; this is because viruses replicate within cells where they are shielded from extracellular contact with circulating antibodies. When APCs phagocytize pathogens and present MHC I-embedded antigens to naïve CD8+ T cells that express complementary TCRs, the CD8+ T cells become activated to proliferate according to clonal selection.

These resulting CTLs then identify non-APCs displaying the same MHC I-embedded antigens (for example, viral proteins)—for example, the CTLs identify infected host cells.

Intracellularly, infected cells typically die after the infecting pathogen replicates to a sufficient concentration and lyses the cell, as numerous viruses do. CTLs attempt to identify and destroy infected cells before the pathogen can replicate and escape, thereby halting the progression of intracellular infections. CTLs also support NK lymphocytes to destroy early cancers. Cytokines secreted by the TH1 response that stimulates macrophages also stimulate CTLs and enhance their ability to identify and destroy infected cells and tumors.

CTLs sense MHC I-embedded antigens by directly interacting with infected cells via their TCRs.

Binding of TCRs with antigens activates CTLs to release perforin and granzyme, degradative enzymes that will induce apoptosis of the infected cell. Recall that this is a similar destruction mechanism to that used by NK cells. In this process, the CTL does not become infected and is not harmed by the secretion of perforin and granzymes. In fact, the functions of NK cells and CTLs are complementary and maximize the removal of infected cells, as illustrated in Figure If the NK cell cannot identify the “missing self” pattern of down-regulated MHC I molecules, then the CTL can identify it by the complicated of MHC I with foreign antigens, which signals “altered self.” Similarly, if the CTL cannot detect antigen-embedded MHC I because the receptors are depleted from the cell surface, NK cells will destroy the cell instead.

CTLs also emit cytokines, such as interferons, that alter surface protein expression in other infected cells, such that the infected cells can be easily identified and destroyed. Moreover, these interferons can also prevent virally infected cells from releasing virus particles.

Based on what you know about MHC receptors, why do you ponder an organ transplanted from an incompatible donor to a recipient will be rejected?

Plasma cells and CTLs are collectively called effector cells: they represent differentiated versions of their naïve counterparts, and they are involved in bringing about the immune defense of killing pathogens and infected host cells.

Learning Objectives

By the finish of this section, you will be capable to:

  1. Compare and contrast adaptive and innate immunity
  2. Describe cell-mediated immune response and humoral immune response
  3. Explain adaptive immunity
  4. Describe immune tolerance

The innate and adaptive immune responses discussed thus far comprise the systemic immune system (affecting the whole body), which is distinct from the mucosal immune system.

Mucosal immunity is formed by mucosa-associated lymphoid tissue, which functions independently of the systemic immune system, and which has its own innate and adaptive components. Mucosa-associated lymphoid tissue (MALT), illustrated in Figure , is a collection of lymphatic tissue that combines with epithelial tissue lining the mucosa throughout the body. This tissue functions as the immune barrier and response in areas of the body with direct contact to the external environment. The systemic and mucosal immune systems use numerous of the same cell types. Foreign particles that make their way to MALT are taken up by absorptive epithelial cells called M cells and delivered to APCs located directly under the mucosal tissue.

M cells function in the transport described, and are located in the Peyer’s patch, a lymphoid nodule. APCs of the mucosal immune system are primarily dendritic cells, with B cells and macrophages having minor roles. Processed antigens displayed on APCs are detected by T cells in the MALT and at various mucosal induction sites, such as the tonsils, adenoids, appendix, or the mesenteric lymph nodes of the intestine. Activated T cells then migrate through the lymphatic system and into the circulatory system to mucosal sites of infection.

MALT is a crucial component of a functional immune system because mucosal surfaces, such as the nasal passages, are the first tissues onto which inhaled or ingested pathogens are deposited.

The mucosal tissue includes the mouth, pharynx, and esophagus, and the gastrointestinal, respiratory, and urogenital tracts.

The immune system has to be regulated to prevent wasteful, unnecessary responses to harmless substances, and more importantly so that it does not attack “self.” The acquired ability to prevent an unnecessary or harmful immune response to a detected foreign substance known not to cause disease is described as immune tolerance. Immune tolerance is crucial for maintaining mucosal homeostasis given the tremendous number of foreign substances (such as food proteins) that APCs of the oral cavity, pharynx, and gastrointestinal mucosa encounter.

Immune tolerance is brought about by specialized APCs in the liver, lymph nodes, little intestine, and lung that present harmless antigens to an exceptionally diverse population of regulatory T (Treg) cells, specialized lymphocytes that suppress local inflammation and inhibit the secretion of stimulatory immune factors. The combined result of Treg cells is to prevent immunologic activation and inflammation in undesired tissue compartments and to permit the immune system to focus on pathogens instead. In addition to promoting immune tolerance of harmless antigens, other subsets of Treg cells are involved in the prevention of the autoimmune response, which is an inappropriate immune response to host cells or self-antigens.

What happens when you own an allergy ap bio

Another Treg class suppresses immune responses to harmful pathogens after the infection has cleared to minimize host cell damage induced by inflammation and cell lysis.


Mucosal Surfaces and Immune Tolerance

If the pathogen is never encountered again during the individual’s lifetime, B and T memory cells will circulate for a few years or even several decades and will gradually die off, having never functioned as effector cells. However, if the host is re-exposed to the same pathogen type, circulating memory cells will immediately differentiate into plasma cells and CTLs without input from APCs or TH cells.

One reason the adaptive immune response is delayed is because it takes time for naïve B and T cells with the appropriate antigen specificities to be identified and activated. Upon reinfection, this step is skipped, and the result is a more rapid production of immune defenses. Memory B cells that differentiate into plasma cells output tens to hundreds-fold greater antibody amounts than were secreted during the primary response, as the graph in Figure illustrates. This rapid and dramatic antibody response may stop the infection before it can even become established, and the individual may not realize they had been exposed.

Vaccination is based on the knowledge that exposure to noninfectious antigens, derived from known pathogens, generates a mild primary immune response.

The immune response to vaccination may not be perceived by the host as illness but still confers immune memory. When exposed to the corresponding pathogen to which an individual was vaccinated, the reaction is similar to a secondary exposure.

What happens when you own an allergy ap bio

Because each reinfection generates more memory cells and increased resistance to the pathogen, and because some memory cells die, certain vaccine courses involve one or more booster vaccinations to mimic repeat exposures: for instance, tetanus boosters are necessary every ten years because the memory cells only live that long.

A subset of T and B cells of the mucosal immune system differentiates into memory cells just as in the systemic immune system. Upon reinvasion of the same pathogen type, a pronounced immune response occurs at the mucosal site where the original pathogen deposited, but a collective defense is also organized within interconnected or adjacent mucosal tissue.

For instance, the immune memory of an infection in the oral cavity would also elicit a response in the pharynx if the oral cavity was exposed to the same pathogen.


Vaccinologist

Vaccination (or immunization) involves the delivery, generally by injection as shown in Figure , of noninfectious antigen(s) derived from known pathogens. Other components, called adjuvants, are delivered in parallel to assist stimulate the immune response. Immunological memory is the reason vaccines work. Ideally, the effect of vaccination is to elicit immunological memory, and thus resistance to specific pathogens without the individual having to experience an infection.

Vaccinologists are involved in the process of vaccine development from the initial thought to the availability of the completed vaccine.

This process can take decades, can cost millions of dollars, and can involve numerous obstacles along the way. For instance, injected vaccines stimulate the systemic immune system, eliciting humoral and cell-mediated immunity, but own little effect on the mucosal response, which presents a challenge because numerous pathogens are deposited and replicate in mucosal compartments, and the injection does not provide the most efficient immune memory for these disease agents. For this reason, vaccinologists are actively involved in developing new vaccines that are applied via intranasal, aerosol, oral, or transcutaneous (absorbed through the skin) delivery methods. Importantly, mucosal-istered vaccines elicit both mucosal and systemic immunity and produce the same level of disease resistance as injected vaccines.

Currently, a version of intranasal influenza vaccine is available, and the polio and typhoid vaccines can be istered orally, as shown in Figure Similarly, the measles and rubella vaccines are being adapted to aerosol delivery using inhalation devices.

Eventually, transgenic plants may be engineered to produce vaccine antigens that can be eaten to confer disease resistance. Other vaccines may be adapted to rectal or vaginal application to elicit immune responses in rectal, genitourinary, or reproductive mucosa. Finally, vaccine antigens may be adapted to transdermal application in which the skin is lightly scraped and microneedles are used to pierce the outermost layer. In addition to mobilizing the mucosal immune response, this new generation of vaccines may finish the anxiety associated with injections and, in turn, improve patient participation.

Although the immune system is characterized by circulating cells throughout the body, the regulation, maturation, and intercommunication of immune factors happen at specific sites.

The blood circulates immune cells, proteins, and other factors through the body. Approximately percent of every cells in the blood are leukocytes, which encompass monocytes (the precursor of macrophages) and lymphocytes. The majority of cells in the blood are erythrocytes (red blood cells).



Further information on poison ivy.

See Case studies in immunology — a clinical companion by Fred S. Rosen and Raif S. Geha, Garland Publishing Inc., (Case 6, contact hypersensitivity). Further information on allergy and hypersensitivity, and the underlying mechanisms, can be found in any textbook of immunology. For a discussion of corticosteroids, see a physiology book, such as the current edition of the Review of Medical Physiology by William F.

Ganong, Appleton and Lange.

Godfrey, H. P., H. Baer, and R. C. Watkins. Delayed hypersensitivity to catechols. V. Absorption and distribution of substances related to poison ivy extracts and their relation to the induction of sensitization and tolerance. J. Immunol. (1)

Here are some relevant web sites:

  1. Poison Ivy and Poison Oak Products at Wayne State U. There’s a excellent list of links here!
  2. Excellent photo at the PLANTS TOXIC TO ANIMALS site of the U Illinois, Urbana-Champaign.

  3. Poison ivy, sumac, and oak by the American Academy of Dermatology. Includes what to do and common myths.
  4. An excellent photo of the red-leafed stage is provided at the Cornell University Poisonous Plants Sheet.
  5. Camper with a rash by Lewis Nelson, M.D., Yale University School of Medicine. Clinical case study with list of plant species and discussion of alternative treatments.
  6. Contact dermatitis home sheet by A. P. Truett, III, M.D. at Vanderbilt University. 4-tertiary-butylcatechol is an industrial chemical which causes contact dermatitis for some workers exposed to it.

  7. There is a excellent common-sense discussion of the medical side of poison ivy at the Famil-e-docs physicians’ website.
  8. An excellent series of photos in diverse seasons is at the Poison Ivy, Western Poison Oak, Poison Sumac site by Gerald A.

    What happens when you own an allergy ap bio

    Mulligan of Agriculture and Agri-Food Canada.

  9. Poisonous Plant Database by D. Jesse Wagstaff, DVM (US Food and Drug istration). An extensive bibliography.

This sheet is maintained by Eric Martz.

I would love to add more graphics to this sheet. If you own some to contribute, please contact me.
Final updated March 31,

For me, it was hornets.

One summer afternoon when I was 12, I ran into an overgrown field near a friend’s home and kicked a hornet nest the size of a football. An mad squadron of insects clamped onto my leg; their stings felt love scorching needles.

I swatted the hornets away and ran for assist, but within minutes I realized something else was happening. A constellation of pink stars had appeared around the stings. The hives swelled, and new ones began appearing farther up my legs. I was having an allergic reaction.

My friend’s mom gave me antihistamines and loaded me into her van. We set out for the county hospital, my dread growing as we drove. I was vaguely aware of the horrible things that can happen when allergies run amok. I imagined the hives reaching my throat and sealing it shut.

I lived to tell the tale: my hives subsided at the hospital, leaving behind a lingering fear of hornets.

But an allergy test confirmed that I was sensitive to the insects. Not to honey bees or wasps or yellow jackets. Just the specific type of hornet that had stung me. The emergency room doctor said I might not be so fortunate the next time I encountered a nest of them. She handed me an EpiPen and told me to ram the syringe into my thigh if I was stung again. The epinephrine would lift my blood pressure, open my airway–and perhaps save my life. I’ve been lucky: that afternoon was 35 years ago, and I haven’t encountered a hornet’s nest since.

I lost track of that EpiPen years ago.

Anyone with an allergy has their origin tale, a tale of how they discovered that their immune system goes haywire when some arbitrarily specific molecule gets into their body. There are hundreds of millions of these stories. In the US alone, an estimated 18 million people suffer from hay fever, and food allergies affect millions of American children. The prevalence of allergies in numerous other countries is rising. The list of allergens includes–but is not limited to–latex, gold, pollen (ragweed, cockleweed and pigweed are especially bad), penicillin, insect venom, peanuts, papayas, jellyfish stings, perfume, eggs, the feces of home mites, pecans, salmon, beef and nickel.

Allergies are not simply a biological blunder.

Instead, they’re an essential defense against noxious chemicals.

Once these substances trigger an allergy, the symptoms can run the gamut from annoying to deadly. Hives appear, lips swell. Hay fever brings sniffles and stinging eyes; allergies to food can cause vomiting and diarrhea. For an unlucky minority, allergies can trigger a potentially fatal whole-body reaction known as anaphylactic shock.

The collective burden of these woes is tremendous, yet the treatment options are limited.

EpiPens save lives, but the available long-term treatments offer mixed results to those exhausted by an allergy to mould or the annual release of pollen. Antihistamines can often reduce sufferers’ symptoms, but these drugs also cause drowsiness, as do some other treatments.

We might own more effective treatments if scientists understood allergies, but a maddening web of causes underlies allergic reactions. Cells are aroused, chemicals released, signals relayed. Scientists own only partially mapped the process. And there’s an even bigger mystery underlying this biochemical web: why do we even get allergies at all?

“That is exactly the problem I love,” Ruslan Medzhitov told me recently.

“It’s extremely large, it’s extremely fundamental, and completely unknown.”

Medzhitov and I were wandering through his laboratory, which is located on the top floor of the Anlyan Middle for Medical Research and Education at the Yale School of Medicine. His team of postdocs and graduate students were wedged tight among man-sized tanks of oxygen and incubators full of immune cells. “It’s a mess, but a productive mess,” he said with a shrug. Medzhitov has a boxer’s face–massive, circular, with a wide, flat nose–but he spoke with a soft elegance.

Medzhitov’s mess has been exceptionally productive.

Over the past 20 years, he has made fundamental discoveries about the immune system, for which he has been awarded a string of major prizes. Final year he was the first recipient of the €4 million Else Kröner Fresenius Award. And though Medzhitov hasn’t won a Nobel, numerous of his peers ponder he should have: in , 26 leading immunologists wrote to Nature protesting that Medzhitov’s research had been overlooked for the prize.

Now Medzhitov is turning his attention to a question that could change immunology yet again: why do we get allergies?

No one has a firm answer, but what is arguably the leading theory suggests that allergies are a misfiring of a defense against parasitic worms. In the industrialized world, where such infections are rare, this system reacts in an exaggerated fashion to harmless targets, making us miserable in the process.

Medzhitov thinks that’s incorrect. Allergies are not simply a biological blunder. Instead, they’re an essential defense against noxious chemicals–a defence that has served our ancestors for tens of millions of years and continues to do so today. It’s a controversial theory, Medzhitov acknowledges.

But he’s also confident that history will prove him correct. “I ponder the field will go around in that stage where there’s a lot of resistance to the idea,” he told me. “Until everybody says, ‘Oh yeah, it’s obvious. Of course it works that way.’”

***

The physicians of the ancient world knew about allergies. Three thousand years ago, Chinese doctors described a “plant fever” that caused runny noses in autumn. There is evidence that the Egyptian pharaoh Menes died from the sting of a wasp in BCE.

Two and a half millennia later, the Roman philosopher Lucretius wrote, “What is food to one is to others bitter poison.”

But it was a little more than a century ago when scientists realized that these diverse symptoms are diverse heads on the same hydra. By then researchers had discovered that numerous diseases are caused by bacteria and other pathogens, and that we fight these invaders with an immune system–an army of cells that can unleash deadly chemicals and precisely targeted antibodies. They soon realized that the immune system can also cause harm.

In the early s, the French scientists Charles Richet and Paul Portier were studying how toxins affect the body. They injected little doses of poison from sea anemones into dogs, then waited a week or so before delivering an even smaller dose. Within minutes, the dogs went into shock and died. Instead of protecting the animals from harm, the immune system appeared to make them more susceptible.

Other researchers observed that some medical drugs caused hives and other symptoms.

And this sensitivity increased with exposure–the opposite of the protection that antibodies provided against infectious diseases. The Austrian doctor Clemens von Pirquet wondered how it was that substances entering the body could change the way the body reacted. To describe this response, he coined the expression ‘allergy’, from the Greek words allos (‘other’) and ergon (‘work’).

Two and a half millennia later, the Roman philosopher Lucretius wrote, “What is food to one is to others bitter poison.”

In the decades that followed, scientists discovered that the molecular stages of these reactions were remarkably similar. The process begins when an allergen lands on one of the body’s surfaces–skin, eye, nasal passage, mouth, airway or gut.

These surfaces are loaded with immune cells that act as border sentries. When a sentry encounters an allergen, it first engulfs and demolishes the invader, then decorates its outer surface with fragments of the substance. Next the cell locates some lymph tissue. There it passes on the fragments to other immune cells, which produce a distinctive fork-shaped antibody, known as immunoglobulin E, or IgE.

These antibodies will trigger a response if they encounter the allergen again. The reaction begins when an antibody activates a component of the immune system known as a mast cell, which then blasts out a barrage of chemicals.

Some of these chemicals latch onto nerves, triggering itchiness and coughing. Sometimes mucus is produced. Airway muscles can contract, making it hard to breathe.

This picture, built up in labs over the past century, answered the “how?” part of the allergies mystery. Left unanswered, however, was “why?” And that’s surprising, because the question had a beautiful clear answer for most parts of the immune system. Our ancestors faced a constant assault of pathogens. Natural selection favored mutations that helped them fend off these attacks, and those mutations accumulated to produce the sophisticated defenses we own today.

It was harder to see how natural selection could own produced allergies.

Reacting to harmless things with a huge immune response probably wouldn’t own aided the survival of our ancestors. Allergies are also strangely selective. Only some people own allergies, and only some substances are allergens. Sometimes people develop allergies relatively tardy in life; sometimes childhood allergies vanish. And for decades, nobody could even figure out what IgE was for. It showed no ability to stop any virus or bacteria.

It was as if we evolved one special helpful of antibody just to make us miserable.

Reacting to harmless things with a huge immune response probably wouldn’t own aided the survival of our ancestors.

One early clue came in A parasitologist named Bridget Ogilvie was investigating how the immune system repelled parasitic worms, and she noticed that rats infected with worms produced large amounts of what would later be called IgE. Subsequent studies revealed that the antibodies signaled the immune system to unleash a damaging assault on the worms.

Parasitic worms represent a serious threat–not just to rats, but to humans too. Hookworms can drain off blood from the gut.

What happens when you own an allergy ap bio

Liver flukes can damage liver tissue and cause cancer. Tapeworms can cause cysts in the brain. More than 20 per cent of every people on Ground carry such an infection, most of them in low-income countries. Before modern public health and food safety systems, our ancestors faced a lifelong struggle against these worms, as well as ticks and other parasitic animals.

During the s, several scientists argued forcefully for a link between these parasites and allergies.

Perhaps our ancestors evolved an ability to recognize the proteins on the surface of worms and to reply with IgE antibodies. The antibodies primed immune system cells in the skin and gut to quickly repel any parasite trying to shove its way in. “You’ve got about an hour to react extremely dramatically in order to reduce the chance of these parasites surviving,” said David Dunne, a parasitologist at the University of Cambridge.

According to the worm theory, the proteins of parasitic worms are similar in shape to other molecules we regularly encounter in our lives. If we encounter those molecules, we mount a pointless defense. “Allergy is just an unlucky side-effect of defense against parasitic worms,” says Dunne.

***

When he was an immunologist in training, Medzhitov was taught the worm theory of allergies.

But ten years ago he started to develop doubts. “I was seeing that it doesn’t make sense,” he said. So Medzhitov began thinking about a theory of his own.

Thinking is a large part of Medzhitov’s science. It’s a legacy of his training in the Soviet Union in the s and s, when universities had little equipment and even less interest in producing excellent scientists. For his undergraduate degree, Medzhitov went to Tashkent State University in Uzbekistan. Every autumn the professors sent the students out into the cotton fields to assist take in the harvest.

They worked daily from dawn to dusk. “It was terrible,” said Medzhitov. “If you don’t do that, you get expelled from college.” He recalls sneaking biochemistry textbooks into the fields–and being reprimanded by a department chair for doing so.

Graduate school wasn’t much better. Medzhitov arrived at Moscow State University just as the Soviet regime collapsed. The university was broke, and Medzhitov didn’t own the equipment he needed to run experiments. “I was basically spending every of my time reading and thinking,” Medzhitov told me.

Mostly, he thought about how our bodies perceive the exterior world. We can recognize patterns of photons with our eyes and patterns of air vibrations with our ears.

To Medzhitov, the immune system was another pattern recognition system–one that detected molecular signatures instead of light or sound.

To Medzhitov, the immune system was another pattern recognition system–one that detected molecular signatures instead of light or sound.

As Medzhitov searched for papers on this subject, he came across references to a essay written by Charles Janeway, an immunologist at Yale, titled “Approaching the Asymptote? Evolution and revolution in immunology.” Medzhitov was intrigued and used several months’ of his stipend to purchase a reprint of the paper. It was worth the wait, because the paper exposed him to Janeway’s theories, and those theories would change his life.

At the time, Janeway was arguing that antibodies own a large drawback: it takes days for the immune system to develop an effective antibody against a new invader.

He speculated that the immune system might own another line of defense that could offer faster protection. Perhaps the immune system could use a pattern-recognition system to detect bacteria and viruses quickly, allowing it to immediately launch a response.

Medzhitov had been thinking about the same thing, and he immediately emailed Janeway. Janeway responded, and they began an exchange that would ultimately bring Medzhitov to New Haven, Connecticut, in , to become a postdoctoral researcher in Janeway’s lab. (Janeway died in )

“He turned out to speak extremely little English, and had almost no experience in a wet laboratory,” says Derek Sant’Angelo, who worked in the lab at the time.

Sant’Angelo, now at the Robert Wood Johnson Medical School in New Jersey, recalls coming across Medzhitov at the bench one night. In one hand, Medzhitov held a mechanical pipette. In the other hand, he held a tube of bacteria. Medzhitov needed to use the pipette to remove a few drops of bacteria from the tube and put them on a plate on the lab bench in front of him. “He was slowly looking back and forth from the pipette below to the plate to the bacteria,” says Sant’Angelo. “He knew in theory that the pipette was used to put the bacteria on the plate. But he simply had absolutely no thought how to do it.”

Medzhitov still marvels that Janeway agreed to work with him.

“I ponder that the only reason that he took me in his lab is that nobody else wanted to touch this idea,” he recalled.

With assist from Sant’Angelo and other members of the lab, Medzhitov learned extremely quickly. Soon he and Janeway discovered a new class of sensor on the surface of a certain helpful of immune cell. Confronted with an invader, the sensors would clasp onto the intruder and trigger a chemical alarm that promoted other immune cells to search the area for pathogens to kill. It was a quick, precise way to sense and remove bacterial invaders.

Medzhitov and Janeway’s discovery of the sensors, now known as toll-like receptors, revealed a new dimension to our immune defenses, and has been hailed as a fundamental principle of immunology.

It also helped solve a medical mystery.

“Thirty years ago, it was, ‘Whatever causes septic shock is bad.’ Well, now we know it’s not.”

Infections sometimes produce a catastrophic body-wide inflammation known as sepsis. It is thought to strike around a million people a year in the USA alone, up to half of whom die. For years, scientists thought that a bacterial toxin might cause the immune system to malfunction in this way – but sepsis is actually just an exaggeration of one of the usual immune defenses against bacteria and other invaders. Instead of acting locally, the immune system accidentally responds throughout the body. “What happens in septic shock is that these mechanisms become activated much more strongly than necessary,” said Medzhitov.

“And that’s what kills.”

Medzhitov isn’t driven to do science to cure people; he’s more interested in basic questions about the immune system. But he argues that cures won’t be found if researchers own the incorrect answers for basic questions. Only now that scientists own a clear understanding of the biology underlying sepsis can they develop treatments that target the genuine cause of the condition–the over-reaction of the toll-like receptors. (Tests are ongoing, and the results so far are promising). “Thirty years ago, it was, ‘Whatever causes septic shock is bad.’ Well, now we know it’s not,” said Medzhitov.

***

Medzhitov kept thinking after he and Janeway discovered toll-like receptors.

If the immune system has special sensors for bacteria and other invaders, perhaps it had undiscovered sensors for other enemies. That’s when he started thinking about parasitic worms, IgE and allergies. And when he thought about them, things didn’t add up.

It’s true that the immune system makes IgE when it detects parasitic worms. But some studies propose that IgE isn’t actually essential to fight these invaders. Scientists own engineered mice that can’t make IgE, for instance, and own found that the animals can still mount a defence against parasitic worms. And Medzhitov was sceptical of the thought that allergens mimic parasite proteins. A lot of allergens, such as nickel or penicillin, own no possible counterpart in the molecular biology of a parasite.

The more Medzhitov thought about allergens, the less significant their structure seemed.

Maybe what ties allergens together was not their shape, but what they do.

We know that allergens often cause physical damage. They rip open cells, irritate membranes, slice proteins into tatters.

What happens when you own an allergy ap bio

Maybe, Medzhitov thought, allergens do so much damage that we need a defense against them. “If you ponder of every the major symptoms of allergic reactions–runny noses, tears, sneezing, coughing, itching, vomiting and diarrhoea–all of these things own one thing in common,” said Medzhitov. “They every own to do with expulsion.” Suddenly the distress of allergies took on a new glance. Allergies weren’t the body going haywire; they were the body’s strategy for getting rid of the allergens.

Maybe, Medzhitov thought, allergens do so much damage that we need a defense against them.

As Medzhitov explored this possibility, he found that the thought had surfaced from time to time over the years, only to be buried again.

In , for example, the evolutionary biologist Margie Profet argued that allergies fought toxins. Immunologists dismissed the thought, perhaps because Profet was an outsider. Medzhitov found it hugely helpful. “It was liberating,” he said.

Together with two of his students, Noah Palm and Rachel Rosenstein, Medzhitov published his theory in Nature in . Then he began testing it. First he checked for a link between damage and allergies. He and colleagues injected mice with PLA2, an allergen that’s found in honey-bee venom and tears apart cell membranes.

As Medzhitov had predicted, the animals’ immune systems didn’t reply to PLA2 itself. Only when PLA2 ripped open cells did the immune system produce IgE antibodies.

Another prediction of Medzhitov’s theory was that these antibodies would protect the mice, rather than just make them ill. To test this, Medzhitov and his colleagues followed their initial injection of PLA2 with a second, much bigger dose. If the animals had not previously been exposed to PLA2, the dose sent their body temperature plunging, sometimes fatally. But the mice that had been exposed marshalled an allergic reaction that, for reasons that aren’t yet clear, lessened the impact of the PLA2.

Medzhitov didn’t know it, but on the other side of the country another scientist was running an experiment that would provide even stronger support for his theory.

Stephen Galli, chair of the Pathology Department at Stanford University School of Medicine, had spent years studying mast cells, the enigmatic immune cells that can kill people during allergic reactions. He suspected mast cells may actually assist the body. In , for example, Galli and colleagues found that mast cells destroy a toxin found in viper venom. That discovery led Galli to wonder, love Medzhitov, whether allergies might be protective.

To discover out, Galli and colleagues injected one to two stings’ worth of honey-bee venom into mice, prompting an allergic reaction.

Then they injected the same animals with a potentially lethal dose, to see if the reaction improved the animal’s chance of survival. It did.

What happens when you own an allergy ap bio

What’s more, when Galli’s team injected the IgE antibodies into mice that had never been exposed to the venom, those animals were also protected against a potentially lethal dose.

Medzhitov was delighted to discover Galli’s paper in the same issue of Immunity that carried his own. “It was excellent to see that somebody got the same results using a extremely diverse model. That’s always reassuring,” Medzhitov told me.

Medzhitov predicts that these experiments will show that allergen detection is love a home-alarm system.

Still, the experiments left a lot unanswered. How precisely did the damage caused by the bee venom lead to an IgE response? And how did IgE protect the mice? These are the kinds of questions that Medzhitov’s team is now investigating. He showed me some of the experiments when I visited again final month. We sidled past a hulking new freezer blocking a corridor to slip into a room where Jaime Cullen, a researcher associate in the lab, spends much of her time. She put a flask of pink syrup under a microscope and invited me to glance.

I could see a flotilla of melon-shaped objects.

“These are the cells that cause every the problems,” said Medzhitov. I was looking at mast cells, the key agents of allergic reactions. Cullen is studying how IgE antibodies latch onto mast cells and prime them to become sensitive–or, in some cases, oversensitive–to allergens.

Medzhitov predicts that these experiments will show that allergen detection is love a home-alarm system. “You can detect a burglar, not by recognizing his face, but by a broken window,” he said. The damage caused by an allergen rouses the immune system, which gathers up molecules in the vicinity and makes antibodies to them.

Now the criminal has been identified and can be more easily apprehended next time he tries to break in.

Allergies make a lot more sense in terms of evolution when seen as a home-alarm system, argues Medzhitov. Toxic chemicals, whether from venomous animals or plants, own endless threatened human health. Allergies would own protected our ancestors by flushing out these chemicals. And the discomfort our ancestors felt when exposed to these allergens might own led them to move to safer parts of their environment.

Toxic chemicals own endless threatened human health.

Allergies would own protected our ancestors by flushing out these chemicals.

Like numerous adaptations, allergies weren’t perfect. They lowered the odds of dying from toxins but didn’t eliminate the risk. Sometimes the immune system overreacts dangerously, as Richet and Protier discovered when the second dose of anemone allergen killed the dogs they were experimenting on. And the immune system might sometimes circular up a harmless molecular bystander when it responded to an allergy alarm.

But overall, Medzhitov argues, the benefits of allergies outstripped their drawbacks.

That balance shifted with the rise of modern Western life, he adds. As we created more synthetic chemicals, we exposed ourselves to a wider range of compounds, each of which could potentially cause damage and trigger an allergic reaction. Our ancestors could avoid allergens by moving to the other side of the forest, but we can’t escape so easily. “In this specific case, the environment we’d own to avoid is living indoors,” said Medzhitov.

Scientists are taking this theory extremely seriously. “Ruslan is one of the most distinguished immunologists in the world,” said Galli.

“If he thinks there’s validity to this thought, I ponder it gets a lot of traction.”

Dunne, on the other hand, is skeptical about the thought that Medzhitov’s theory explains every allergies. Medzhitov is underestimating the huge diversity of proteins that Dunne and others are finding on the surface of worms–proteins that could be mimicked by a huge range of allergens in the modern world. “My money’s more on the worm one,” he said.

***

Over the next few years, Medzhitov hopes to persuade skeptics with another experiment.

It’s unlikely to finish the debate, but positive results would bring numerous more people over to his way of thinking. And that might eventually lead to a revolution in the way we treat allergies.

Sitting on Cullen’s lab bench is a plastic box that houses a pair of mice. There are dozens more of these boxes in the basement of their building. Some of the mice are ordinary, but others are not: using genetic engineering techniques, Medzhitov’s team has removed the animals’ ability to make IgE. They can’t get allergies.

Medzhitov would just be happy to get people to stop seeing allergies as a disease, despite the distress they cause.

Medzhitov and Cullen will be observing these allergy-free mice for the next couple of years. The animals may be spared the distress of hay fever caused by the ragweed pollen that will inevitably drift into their box on currents of air. But Medzhitov predicts they will be worse off for it. Unable to fight the pollen and other allergens, they will let these toxic molecules pass into their bodies, where they will damage organs and tissues.

“It’s never been done before, so we don’t know what the consequences will be,” says Medzhitov. But if his theory is correct, the experiment will reveal the invisible shield that allergies provide us.

Even if the experiment works out just as he predicts, Medzhitov doesn’t ponder his ideas about allergies will win out as quickly as his ideas about toll-like receptors.

The thought that allergic reactions are bad is ingrained in the minds of physicians. “There’s going to be more inertia,” he said.

But understanding the purpose of allergies could lead to dramatic changes in how they’re treated. “One implication of our view is that any attempt to completely block allergic defenses would be a bad idea,” he said. Instead, allergists should be learning why a minority of people turn a protective response into a hypersensitive one. “It’s the same as with pain,” said Medzhitov. “No pain at every is deadly; normal pain is good; too much pain is bad.”

For now, however, Medzhitov would just be happy to get people to stop seeing allergies as a disease, despite the distress they cause.

“You’re sneezing to protect yourself. The fact that you don’t love the sneezing, that’s tough luck,” he said, with a slight shrug. “Evolution doesn’t care how you feel.”

Flagstaff High School Pre-AP Biology Syllabus

Ms. Linda S. Lenz

Room

[email protected]

Course website:

Course Overview

The content of this course is aligned with the Arizona Science Standards and the content of instruction is guided by the National Research Council of the National Academy of Science’s Framework for K Science Education and College Board’s AP Biology Curriculum Framework.

This course is structured around the core and component ideas (see below). You will develop essential biology knowledge by applying science practices (see below) through inquiry-style experiences that will provide you with an organizational framework for connecting knowledge from across disciplines into a coherent and scientifically based view of the world. You will develop the habits of mind that are necessary for scientific thinking and that permit you to engage in science in ways that are similar to those used by scientists.

Additionally, we are participating in a program called GK12, which will involve collaboration between our class and Northern Arizona University (NAU) biology PhD candidates. This course is an Alpine Institute designated science class, and as such, will own a place-based emphasis that promotes the development of the following five core values: Inquiry, Community, Stewardship, Critical thinking and Reflection. Students will take part in a service-learning journey to the Arboretum at Flagstaff in September and a second journey to a diverse location (to be determined) will be arranged for the Spring.

Core and Component Ideas in Biology

  1. From Molecules to Organisms: Structures and Processes
  2. Heredity: Inheritance and Variation of Traits
  3. Ecosystems: Interactions, Energy, and Dynamics
  4. Biological Evolution: Unity and Diversity

Science Practices

  1. Pan and implement data collection strategies by selecting the type of data necessary to answer a question, designing a plan for data collection, collecting data, and/or evaluating sources of data.
  2. Engage in scientific questioning by posing, refining, and evaluating scientific questions.
  3. Perform data analysis and assess evidence by searching for patterns and relationships, refining observations and measurements based on these, and assess data presented in data sets in relation to a scientific question.
  4. Justify the use of mathematical routines to solve problems, apply a mathematical routine to a data set, and apply appropriate estimation techniques.
  5. Justify claims using scientific evidence, construct explanations based on evidence, make predictions, assess alternative scientific explanations, and explain why scientific explanations are refined or replaced.
  6. Create, describe, refine, and use scientific representations and models of scientific phenomena to analyze situations or solve problems.
  7. Connect knowledge of phenomena and models across both spatial and temporal scales and join concepts across domains.

Grade Determination

  1. Flagstaff high school has adopted a 80% measurement/performance and 20% practice grade breakdown.
  2. Below you will see how the percentage of points will be awarded within each category, each semester:

Measurement/performance: 4 exams (including semester final) worth % each (50% of category total), 4 quizzes worth % each (30% of category total), 4 examples of performance to include: lab reports/lab quiz/performance rubrics, free response question writing, and case-studies 5% each (20% of category total)

Practice: 4 unit packets worth % each (50% of category total), 10 random homework checks worth 5% each (50% of category total)

*Actual number of assignments within each category may differ from what is planned

Materials Required Each Class Session

Section in a 3-ring binder: unit packet, loose-leaf notebook paper, graph paper, organized class handouts and returned work

Following items kept in a pencil pouch: scientific calculator (i.e.

TI), pencils, eraser, highlighter, four colored pencils (your choice of colors), and dry-erase board marker

*Please let me know if you require assistance acquiring any of the materials listed above

Safety Expectations

Conduct yourself in a responsible manner. Hold food in your backpack, drink only from a sealable water bottle, and hold your work-space clutter-free.

Practice only the lab-specific safety and experimental procedures that are demonstrated during the pre-lab activity. Inform me if you own any allergies, including to antibiotics (antibiotics are used in microbiology labs). We will practice safety in the school courtyards and during excursions to the Francis Short Pond. Failure to follow proper procedures will result in removal from the laboratory and/or outdoor environment.

Classroom Rules

Our classroom practices the school-wide expectations of Focus, Honor, and Success (FHS).

Statement of Academic Integrity Expectations:

Integrity of scholarship is essential for an academic community.

Flagstaff High School expects that students will honor this principle and in so doing protect the validity of Flagstaff High School’s intellectual work. For students, this means that every academic work will be done by the individual to whom it is assigned, without unauthorized aid of any kind.

Classroom Procedures

Start of class – Prior to the bell: pick up materials by the door as you enter, sit according to seating chart, read the posted entrance announcements, setup your desk with every needed materials, and turn off and stow cellphone.

Missing required materials – Prior to the bell, you may enquire to borrow an item from a classmate or your teacher.

During class – Stay focused, on-task, and use your class time efficiently.

Work collaboratively with your peers to practice skills and build understanding.

Absences – You are expected to check the course website’s finish lesson folder () and review the PDF lesson and finish assigned work. See me with questions upon your return. Missed lab experiences will require you to finish an alternate assignment. A missed exam or quiz must be completed during the announced after school make-up session.

Out of class privileges – Each semester, you will be provided with three bathroom passes.

You may earn additional passes through some reasonable compensation. Please alert me if you own a medical need that requires more frequent bathroom trips. Unused passes may be submitted for additional credit at the finish of the semester.

Ending Class – You will be instructed to pack-up (this should take no more than 30 seconds) and class will finish after successful completion of one of several possible ticket-out-the-door activities.

Missing/Late work— Must be completed by the date of the summative assessment (exam) over the content of the work.

Office Hours

Daily –

*If you need to see me before school, please make an appointment so that I know to expect you

Extra credit opportunities: Submit unused bathroom passes at finish of semester, Festival of Science, and Stem Night

Suggested Parent Participation

  1. Become familiar with the support and content offered on the course website ().
  2. View and discuss together with your student ongoing work in the student’s biology packet
  3. Monitor student grades weekly on-line using ParentVUE and communicate questions and concerns via email.
  4. Sign student packet/study-guide at the finish of each unit and confirm that the student has enacted a study plan to prepare for the exams and quizzes.

Core and Component Ideas in Biology from Framework for K Science Education:

Ecosystems: Interactions, Energy, and Dynamics

Interdependent Relationships in Ecosystems

Ecosystems own carrying capacities, which are limits to the numbers of organisms and populations they can support.

These limits result from such factors as the availability of living and nonliving resources and from such challenges as predation, competition, and disease. Organisms would own the capacity to produce populations of grand size were it not for the fact that environments and resources are finite. This fundamental tension affects the abundance (number of individuals) of species in any given ecosystem.

Cycles of Matter and Energy Transfer in Ecosystems

Photosynthesis and cellular respiration (including anaerobic processes) provide most of the energy for life processes.

Plants or algae form the lowest level of the food web. At each link upward in a food web, only a little part of the matter consumed at the lower level is transferred upward, to produce growth and release energy in cellular respiration at the higher level. Given this inefficiency, there are generally fewer organisms at higher levels of a food web, and there is a limit to the number of organisms that an ecosystem can sustain.

The chemical elements that make up the molecules of organisms pass through food webs and into and out of the atmosphere and soil and are combined and recombined in diverse ways.

At each link in an ecosystem, matter and energy are conserved; some matter reacts to release energy for life functions, some matter is stored in newly made structures, and much is discarded. Competition among species is ultimately competition for the matter and energy needed for life. Photosynthesis and cellular respiration are significant components of the carbon cycle, in which carbon is exchanged between the biosphere, atmosphere, oceans, and geosphere through chemical, physical, geological, and biological processes.

Ecosystem Dynamics, Functioning, and Resilience

A complicated set of interactions within an ecosystem can hold its numbers and types of organisms relatively constant over endless periods of time under stable conditions.

If a modest biological or physical disturbance to an ecosystem occurs, it may return to its more or less original status (i.e., the ecosystem is resilient), as opposed to becoming a extremely diverse ecosystem. Extreme fluctuations in conditions or the size of any population, however, can challenge the functioning of ecosystems in terms of resources and habitat availability. Moreover, anthropogenic changes (induced by human activity) in the environment—including habitat destruction, pollution, introduction of invasive species, overexploitation, and climate change—can disrupt an ecosystem and threaten the survival of some species.

Social Interactions and Group Behavior

Animals, including humans, having a strong drive for social affiliation with members of their own species and will suffer, behaviorally as well as physiologically, if reared in isolation, even if every of their physical needs are met.

Some forms of affiliation arise from the bonds between offspring and parents. Other groups form among peers. Group behavior has evolved because membership can increase the chances of survival for individuals and their genetic relatives.

From Molecules to Organisms: Structures and Processes

Structure and Function

Systems of specialized cells within organisms assist them act out the essential functions of life, which involve chemical reactions that take put between diverse types of molecules, such as water, proteins, carbohydrates, lipids, and nucleic acids.

Every cells contain genetic information in the form of DNA molecules. Genes are regions in the DNA that contain the instructions that code for the formation of proteins, which carry out most of the work of cells. Multicellular organisms own a hierarchical structural organization, in which any one system is made up of numerous parts and is itself a component of the next level. Feedback mechanisms maintain a living system’s internal conditions within certain limits and mediate behaviors, allowing it to remain alive and functional even as external conditions change within some range.

Exterior that range (e.g., at a too high or too low external temperature, with too little food or water available), the organism cannot survive. Negative feedback mechanisms are used to maintain homeostasis.

Growth and Development of Organisms

In multicellular organisms, individual cells grow and then divide via a process called mitosis, thereby allowing the organism to grow. The organism begins as a single cell (fertilized egg) that divides successively to produce numerous cells, with each parent cell passing identical genetic material (two variants of each chromosome pair) to both daughter cells.

As successive subdivisions of an embryo’s cells happen, programmed genetic instructions and little differences in their immediate environments activate or inactivate diverse genes, which cause the cells to develop differently—a process called differentiation. Cellular division and differentiation produce and maintain a complicated organism, composed of systems of tissues and organs that work together to meet the needs of the whole organism.

In sexual reproduction, a specialized type of cell division called meiosis occurs that results in the production of sex cells, such as gametes in animals (sperm and eggs), which contain only one member from each chromosome pair in the parent cell

Organization for Matter and Energy Flow in Organisms

The process of photosynthesis converts light energy to stored chemical energy by converting carbon dioxide plus water into sugars plus released oxygen. The sugar molecules thus formed contain carbon, hydrogen, and oxygen; their hydrocarbon backbones are used to make amino acids and other carbon-based molecules that can be assembled into larger molecules (such as proteins or DNA), used for example to form new cells.

As matter and energy flow through diverse organizational levels of living systems, chemical elements are recombined in diverse ways to form diverse products. As a result of these chemical reactions, energy is transferred from one system of interacting molecules to another. For example, aerobic (in the presence of oxygen) cellular respiration is a chemical process in which the bonds of food molecules and oxygen molecules are broken and new compounds are formed that can transport energy to muscles. Anaerobic (without oxygen) cellular respiration follows a diverse and less efficient chemical pathway to provide energy in cells.

Cellular respiration also releases the energy needed to maintain body temperature despite ongoing energy loss to the surrounding environment. Matter and energy are conserved in each change. This is true of every biological systems, from individual cells to ecosystems.

Information Processing

In complicated animals, the brain is divided into several distinct regions and circuits, each of which primarily serves dedicated functions, such as visual perception, auditory perception, interpretation of perceptual information, guidance of motor movement, and decision making about actions to take in the event of certain inputs.

In addition, some circuits give rise to emotions and memories that motivate organisms to seek rewards, avoid punishments, develop fears, or form attachments to members of their own species and, in some cases, to individuals of other species (e.g., mixed herds of mammals, mixed flocks of birds). The integrated functioning of every parts of the brain is significant for successful interpretation of inputs and generation of behaviors in response to them.

Heredity: Inheritance and Variation of Traits

Inheritance of Traits

In every organisms the genetic instructions for forming species’ characteristics are carried in the chromosomes.

Each chromosome consists of a single extremely endless DNA molecule, and each gene on the chromosome is a specific segment of that DNA. The instructions for forming species’ characteristics are carried in DNA. Every cells in an organism own the same genetic content, but the genes used (expressed) by the cell may be regulated in diverse ways. Not every DNA codes for a protein; some segments of DNA are involved in regulatory or structural functions, and some own no as-yet known function.

Variation of Traits

The information passed from parents to offspring is coded in the DNA molecules that form the chromosomes.

In sexual reproduction, chromosomes can sometimes swap sections during the process of meiosis (cell division), thereby creating new genetic combinations and thus more genetic variation. Although DNA replication is tightly regulated and remarkably precise, errors do happen and result in mutations, which are also a source of genetic variation. Environmental factors can also cause mutations in genes, and viable mutations are inherited. Environmental factors also affect expression of traits, and hence affect the probability of occurrences of traits in a population. Thus the variation and distribution of traits observed depend on both genetic and environmental factors.

Biological Evolution: Unity and Diversity

Evidence of Common Ancestry and Diversity

Genetic information, love the fossil record, also provides evidence of evolution.

DNA sequences vary among species, but there are numerous overlaps; in fact, the ongoing branching that produces multiple lines of descent can be inferred by comparing the DNA sequences of diverse organisms. Such information is also derivable from the similarities and differences in amino acid sequences and from anatomical and embryological evidence.

Natural Selection

Natural selection occurs only if there is both (1) variation in the genetic information between organisms in a population and (2) variation in the expression of that genetic information—that is, trait variation—that leads to differences in performance among individuals.

The traits that positively affect survival are more likely to be reproduced and thus are more common in the population.

Adaptation

Natural selection is the result of four factors: (1) the potential for a species to increase in number, (2) the genetic variation of individuals in a species due to mutation and sexual reproduction, (3) competition for an environment’s limited supply of the resources that individuals need in order to survive and reproduce, and (4) the ensuing proliferation of those organisms that are better capable to survive and reproduce in that environment. Natural selection leads to adaptation—that is, to a population dominated by organisms that are anatomically, behaviorally, and physiologically well suited to survive and reproduce in a specific environment.

That is, the differential survival and

Biodiversity and Humans

Biodiversity is increased by the formation of new species (speciation) and decreased by the loss of species (extinction). Biological extinction, being irreversible, is a critical factor in reducing the planet’s natural capital.

Humans depend on the living world for the resources and other benefits provided by biodiversity. But human activity is also having adverse impacts on biodiversity through overpopulation, overexploitation, habitat destruction, pollution, introduction of invasive species, and climate change. These problems own the potential to cause a major wave of biological extinctions—as numerous species or populations of a given species, unable to survive in changed environments, die out—and the effects may be harmful to humans and other living things.

Thus sustaining biodiversity so that ecosystem functioning and productivity are maintained is essential to supporting and enhancing life on Ground. Sustaining biodiversity also aids humanity by preserving landscapes of recreational or inspirational value.

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A.P. BioSeason 1

A.P. Bio knows what you’re expecting: A bitter, caustic intellectual who, after being forced into a teaching occupation he finds beneath him, discovers a newfound passion and a unused sense of optimism thanks to the wide-eyed wonder of his students. It’s to creator Mike O’Brien’s benefit, then, that the pilot not only demolishes those tropes, but acknowledges its own subversion via an opening monologue that establishes:

1) The protagonist: Jack Griffin, an “award-winning philosophy scholar.”

2) The setting: A high school in Toledo, where Jack is living in his “dead mom’s apartment.”

3) The setup: Jack, for reasons he “won’t go into,” has a “free year” and is “killing a little bit of time” by teaching Advanced Placement Biology.

4) The plot: Or, seemingly, lack thereof.

“This won’t be one of those things where, over the course of a year, I secretly teach it to you,” Jack clarifies. “This also won’t be one of those things where I finish up learning more from you than you do for me.”

5) The goal: “I’m going to spend the majority of my time mentally breaking my nemesis with the ultimate goal of taking his occupation as the head of Stanford philosophy,” he cleanly lays out. “And then I’m going to own sex with as numerous women as I possibly can throughout the state of California.”

What generally takes an entire episode to establish is here laid out, in extremely self-aware fashion, before the opening credits.

This show, it asserts, is not love the others. This expediency, coupled with that smirking self-awareness and a healthy honor for the audience, constitutes everything that’s clicking with A.P. Bio’s pilot episode, which is brisk, amusing, and reliably surprising without ever really telling much of a tale.

What we get instead are scraps of narrative: Jack goes on a date with his high school ex (who he plans to “bang as hard as I can”); his bad behavior inspires a student to act out; Jack helps that same student out with a bully (sorta); he manipulates “laid back” Principal Durbin (Patton Oswalt); and he tasks his biology students with “catfishing” Miles on .

There’s no lasting consequence to any of these stories, nor is there the sense that anything at every has really been accomplished. It’s as if by laying out the show’s overarching narrative in the beginning, the show is absolving itself of committing to any narrative structure.

This isn’t a complaint, necessarily. Not yet, at least. Because A.P. Bio, more than most sitcoms, already seems to own a firm grasp on what makes it amusing. The foul, colorful absurdity of O’Brien, the weirdo behind SNL’s Ass Dan and that “Smash Mouth in the closet” bit, makes for a fine pairing with Glenn Howerton, whose Jack is only a few steps removed from the blunt cruelty he honed as Dennis across 12 seasons of It’s Always Sunny in Philadelphia.

What happens when you own an allergy ap bio

Howerton’s mania is dialed below here (well, slightly; he still threatens a guy with a crowbar at one point), but his acid tongue, sneering superiority, and general inappropriateness remains a delight.

If there’s one sequence that best marries O’Brien and Howerton’s comic sensibilities, it’s when the students stage a surprise “rap” as a means of convincing Jack to actually teach them something. The scene itself, which serves as a subversion of Dangerous Minds-type tropes, is pure O’Brien, but it’s Howerton’s straight-faced dressing below of the kids that truly elevates the joke.

“Don’t ever surprise me with a rap,” he scolds. “Don’t ever rap about learning.” Later, after discovering a saxophone player hiding in the closet, he explains as if in mid-lecture that “saxophones do not belong in rap music.” What a hilarious, absurd takeaway from such a discovery.

The scene also points to a compelling question: How do these kids actually feel about Jack?

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With the rap, they seem to be urging him to make an effort to teach them. Yet, later, when he has conjure up “catfishing” scenarios for Miles, they seem to relish the chance to engage in inappropriate, non-Bio related behavior. So, are they on his side? Or no? If the kids desire him to teach, that serves as yet another clever subversion, this time of the fictional teacher’s timeworn effort to make students care about learning. Turn that around and you’ve got a unique conflict. There’s fruit there, should O’Brien select to pursue it.

And the show could use more conflict. We know Jack wants to get a bigger, better teaching occupation while also smiting his rival and getting laid, but those are goals that, in numerous ways, exist independently of every the characters at the school. As a pilot, the likes of which exist to bring us into a world, every of that is fine. But humor alone won’t be capable to sustain a series that doesn’t embrace its ensemble.

Stray observations

  1. I didn’t get a chance to mention them above, as, well, they didn’t really do much, but I’m looking forward to more from the trio of Michelle (Jean Villepique), Stef (Lyric Lewis), and Mary (Mary Sohn), every of whom made the most of their minimal screen time. The nonchalance with which Michelle says her husband sends her “butt selfies” makes me extremely, extremely excited to study more about this marriage.
  2. I do love that the only reason we’re given for why Jack got fired from Harvard was because he got into a fight with an unnamed “old person.” I honestly wouldn’t be mad if we found out no other details.

  3. Speaking of nonchalance: Jack casually confirming to Durbin that, yes, there is a raccoon on the second floor of his home was a fine moment of standalone absurdity.
  4. A extremely Dennis line: “As I mentioned, I’ve been trying to mentally break my nemesis, Miles Leonard. He currently has the occupation that is rightfully mine and I desire it back. He seems to be winning at the moment, but by the time we’re done with him he’ll be in a looney bin begging for death.”
  5. Also, what, does he only teach the one class?

  6. Obviously, there’s plenty of comparisons to be made to both Eastbound & Down and Vice Principals, but the tones of those shows and this one are beautiful wildly diverse, as is Howerton’s style versus Danny McBride’s, so I probably won’t be going there too often.
  7. God willing, I’ll be with you for the entirety of A.P. Bio’s first season, so do comment, question, and engage. As a longtime Sunny (and Howerton) fan, I’m extremely excited about this series and would not mind whatsoever if a portion of the comments is devoted to Dennis quotes.

  8. I’m not familiar enough with high school academia, but a fired Harvard philosophy professor can’t just waltz into a school and start teaching a subject in which they own no experience, correct? You’d ponder he’d be teaching community college or something. While A.P. Bio’s pilot has proven itself blessedly allergic to exposition, some background as to how Jack got the gig would be much appreciated.
  9. “I will literally beat you up with my adult muscles.”

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Randall Colburn is The A.V. Club’s Internet Culture Editor. He lives in Chicago, occasionally writes plays, and was a talking head in Best Worst Movie, the documentary about Troll 2.

The adaptive, or acquired, immune response takes days or even weeks to become established—much longer than the innate response; however, adaptive immunity is more specific to pathogens and has memory.

Adaptive immunity is an immunity that occurs after exposure to an antigen either from a pathogen or a vaccination. This part of the immune system is activated when the innate immune response is insufficient to control an infection. In fact, without information from the innate immune system, the adaptive response could not be mobilized. There are two types of adaptive responses: the cell-mediated immune response, which is carried out by T cells, and the humoral immune response, which is controlled by activated B cells and antibodies. Activated T cells and B cells that are specific to molecular structures on the pathogen proliferate and attack the invading pathogen.

Their attack can kill pathogens directly or secrete antibodies that enhance the phagocytosis of pathogens and disrupt the infection. Adaptive immunity also involves a memory to provide the host with long-term protection from reinfection with the same type of pathogen; on re-exposure, this memory will facilitate an efficient and quick response.

Unlike NK cells of the innate immune system, B cells (B lymphocytes) are a type of white blood cell that gives rise to antibodies, whereas T cells (T lymphocytes) are a type of white blood cell that plays an significant role in the immune response.

T cells are a key component in the cell-mediated response—the specific immune response that utilizes T cells to neutralize cells that own been infected with viruses and certain bacteria. There are three types of T cells: cytotoxic, helper, and suppressor T cells. Cytotoxic T cells destroy virus-infected cells in the cell-mediated immune response, and helper T cells frolic a part in activating both the antibody and the cell-mediated immune responses. Suppressor T cells deactivate T cells and B cells when needed, and thus prevent the immune response from becoming too intense.

An antigen is a foreign or “non-self” macromolecule that reacts with cells of the immune system.

Not every antigens will provoke a response. For instance, individuals produce innumerable “self” antigens and are constantly exposed to harmless foreign antigens, such as food proteins, pollen, or dust components. The suppression of immune responses to harmless macromolecules is highly regulated and typically prevents processes that could be damaging to the host, known as tolerance.

The innate immune system contains cells that detect potentially harmful antigens, and then inform the adaptive immune response about the presence of these antigens. An antigen-presenting cell (APC) is an immune cell that detects, engulfs, and informs the adaptive immune response about an infection.

When a pathogen is detected, these APCs will phagocytose the pathogen and digest it to form numerous diverse fragments of the antigen. Antigen fragments will then be transported to the surface of the APC, where they will serve as an indicator to other immune cells. Dendritic cells are immune cells that process antigen material; they are present in the skin (Langerhans cells) and the lining of the nose, lungs, stomach, and intestines. Sometimes a dendritic cell presents on the surface of other cells to induce an immune response, thus functioning as an antigen-presenting cell. Macrophages also function as APCs.

Before activation and differentiation, B cells can also function as APCs.

After phagocytosis by APCs, the phagocytic vesicle fuses with an intracellular lysosome forming phagolysosome. Within the phagolysosome, the components are broken below into fragments; the fragments are then loaded onto MHC class I or MHC class II molecules and are transported to the cell surface for antigen presentation, as illustrated in Figure Note that T lymphocytes cannot properly reply to the antigen unless it is processed and embedded in an MHC II molecule.

APCs express MHC on their surfaces, and when combined with a foreign antigen, these complexes signal a “non-self” invader. Once the fragment of antigen is embedded in the MHC II molecule, the immune cell can reply. Helper T- cells are one of the main lymphocytes that reply to antigen-presenting cells. Recall that every other nucleated cells of the body expressed MHC I molecules, which signal “healthy” or “normal.”


Primary Centers of the Immune System


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