Get Complete Information on Infections and Autoimmunity

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There are intimate links between infectious agents (viruses, bacteria, etc) and autoimmunity.

Microbial attack may be one of the key environmental factors that trigger autoimmune disease. Although the microorganisms present are too low to be detected even by the most sensitive clinical tests, they are detected by the immune system.

Even the most virulent microbes fail to cause disease in such low quantity, but the immune system attempts to flush out and destroy them, which could cause extensive damage to apparently normal tissues.

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Exposure of auto – antigens on the surface of microbial cells is another possibility for induction of autoimmune reactions. Molecular mimicry (resemblance of auto antigens) is another possibility for induction of autoimmune reactions.

Some times antigens present on the foreign agents show resemblances with the host’s auto antigens hence antibodies produced against the foreign agents’ cross-react with auto cell antigens leading to damage their own cells.

Inflammation of valvular endocardium in acute rheumatic fever, hemolytic anemia in syphilis are very good examples for this kind of auto immunity. Cross reaction of antibodies produced against Streptococus bacteria in rheumatic fever, with cells of cardiac valves leads to their dysfunction resulting in dilation and congestive heart failure.

Cross reaction of antibodies produced against Treponema palidum antigens with certain erythrocyte blood group antigens results in the destruction of RBC’s leading to hemolytic anemia.

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Adjuvants (usually bacterial) when administered with self-antigens activate the innate immune response similar to pathogen-specific manner; this process results in organ-specific autoimmune disease in animal models.

Microorganisms are likely to provide not only the adjuvant effect to stimulate the immune response but also the damage necessary to make self-antigens available to the immune system, resulting in autoimmune disease.

Viruses also induce autoimmune diseases through polyclonal activation of lymphocytes.

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