What is the difference between allergies and autoimmune diseases

The human immune system typically produces both T cells and B cells that are capable of being reactive with self-antigens, but these self-reactive cells are generally either killed prior to becoming athletic within the immune system, placed into a state of anergy (silently removed from their role within the immune system due to over-activation), or removed from their role within the immune system by regulatory cells. When any one of these mechanisms fail, it is possible to own a reservoir of self-reactive cells that become functional within the immune system.

The mechanisms of preventing self-reactive T cells from being created takes put through negative selection process within the thymus as the T cell is developing into a mature immune cell.

Some infections, such as Campylobacter jejuni, own antigens that are similar (but not identical) to our own self-molecules. In this case, a normal immune response to C. jejuni can result in the production of antibodies that also react to a lesser degree with gangliosides of myelin sheath surrounding peripheral nerves’ axons (i.e., Guillain–Barré).

A major understanding of the underlying pathophysiology of autoimmune diseases has been the application of genome wide association scans that own identified a degree of genetic sharing among the autoimmune diseases.[10]

Autoimmunity, on the other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T cells), with or without damage or pathology resulting from it.[11] This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a specific tissue in diverse places (e.g.

What is the difference between allergies and autoimmune diseases

Goodpasture’s disease which may affect the basement membrane in both the lung and the kidney).

There are numerous theories as to how an autoimmune disease state arises.

What is the difference between allergies and autoimmune diseases

Some common ones are listed under.

Altered glycan theory

According to this theory the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity own alterations in their glycosylation profile such that a proinflammatory immune response is favored.

What is the difference between allergies and autoimmune diseases

It is further hypothesized that individual autoimmune diseases will own unique glycan signatures.[14]

Molecular mimicry

The concept of molecular mimicry describes a situation in which a foreign antigen can initiate an immune response in which a T or B cell component cross-recognizes self. The cross reactive immune response is responsible for the autoimmune disease state.[13] Cross-reactive immune responses to self were first described for antibodies.

Cryptic determinants/molecular sequestration

Although it is possible for a potential autoantigen to be spatially sequestered in an immune privileged site within the body (e.g. the eye), mechanisms exist to express even these antigens in a tolerogenic fashion to the immune system.

What is the difference between allergies and autoimmune diseases

However, it is impossible to induce tolerance (immune unresponsiveness) to every aspects of an autoantigen. This is because under normal physiologic conditions some regions of a self-antigen are not expressed at a sufficient level to induce tolerance. These poorly displayed areas of an antigen are called «cryptic determinants.» The immune system maintains a high-affinity repertoire to the cryptic self because the presentation of these determinants was insufficient to induce strong tolerance.[12]

Hygiene hypothesis

According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune or allergic conditions such as asthma.[15]


Research

In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems.

In autoimmunity, the patient’s immune system is activated against the body’s own proteins.

What is the difference between allergies and autoimmune diseases

In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, leading to tissue damage.

Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach.[21][22][23] There is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies own the capacity to maintain their own production.[24]

Stem cell transplantation is being studied and has shown promising results in certain cases.[25]


Epidemiology

The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al.

They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million.[18] Jacobson’s work was updated by Hayter & Cook in 2012.[19] This study used Witebsky’s postulates, as revised by Rose & Bona,[20] to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that numerous people own more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females.[19]


History

Traditionally it was believed that the immune system was unable to react against the body’s own tissues, a concept described by the German immunologist Paul Ehrlich as «horror autotoxicus».

In 1904 this theory was challenged by the discovery of a substance in the serum of patients with paroxysmal freezing hemoglobinuria that reacted with red blood cells.[26]


Diagnosis

For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky’s postulates (first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994):[16][17]

  1. Indirect evidence based on reproduction of the autoimmune disease in experimental animals
  2. Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white blood cells
  3. Circumstantial evidence from clinical clues


Signs and symptoms

Autoimmune diseases own a wide variety of diverse effects.

What is the difference between allergies and autoimmune diseases

They do tend to own one of three characteristic pathological effects which characterize them as autoimmune diseases:[6]

  • Altered organ growth
  • Damage to or destruction of tissues
  • Altered organ function

It has been estimated that autoimmune diseases are among the leading causes of death among women in the United States in every age groups up to 65 years.[7]

A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening.[citation needed]

There are more than 80 illnesses caused by autoimmunity.[8]

It has been estimated that autoimmune diseases are among the leading causes of death among women in the United States in every age groups up to 65 years.[7]

A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening.[citation needed]

There are more than 80 illnesses caused by autoimmunity.[8]


Causes

The cause is generally unknown.[3] Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors.[1] There are more than 100 autoimmune diseases.[9] Some common diseases that are generally considered autoimmune include celiac disease, diabetes mellitus type 1, Graves’ disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus.[1][4]


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