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Infection, vaccines and other environmental autoimmunity factors

Infection, vaccines and other environmental autoimmunity factors

Journal Autoimmunity
Molina V (1,2), Shoenfeld Y. (1,2,3)
(1) Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel, (2) The Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel, and (3) Incumbent of the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases, Tel-Aviv University, Tel-Aviv, Israel


Abstract

The etiology of autoimmune diseases is not yet clear, but genetic, immunological, hormonal and environmental factors are considered important triggers. Very often autoimmunity is not followed by clinical symptoms unless an additional event such as an environmental factor favors a manifest expression.

Many environmental factors are known to influence the immune system and may play a role as trigger factors in the autoimmune mosaic. Infections: bacterial, viral and parasitic infections are known to induce and exacerbate autoimmune diseases, mainly through the mechanism of molecular mimicry. This has been studied for some syndromes such as the association between SLE and EBV infection, pediatric autoimmune neuropsychiatric conditions associated with streptococcal infection and more. Vaccines, in several reports, have been found to be temporarily followed by a new onset of autoimmune diseases. The same mechanisms that act in the host's infectious infection also apply to the host's response to vaccination. It has been accepted for diphtheria and toxoid, polio and measles and GBS vaccines. This theory has also been accepted for MMR vaccination and the development of autoimmune thrombocytopenia, MS has been associated with vaccination against HBV. Occupational exposures and other chemical exposures are considered as trigger factors for autoimmunity. There is still a debate about the role of silicone implants in the induction of a disease similar to scleroderma. Not only chemicals and foreign agents have been associated with autoimmunity induction, but also with intrinsic hormonal exposure, such as estrogen. This could explain sexual dimorphism in autoimmunity. A better understanding of these environmental risk factors will probably lead to an explanation of the mechanisms of onset and progression of autoimmune diseases and could lead to effective preventive involvement in specific high risk groups. Hence, extensive medical history work should be done to diagnose a new patient with an autoimmune disease.


Conclusions

Most autoimmune connective tissue diseases have no known etiological agents. Nonetheless, some medicines and environmental or occupational factors have undoubtedly been shown to exacerbate a known autoimmune disease or trigger the onset of a syndrome that closely resembles one of the proven diseases. Hence, extensive medical history work should be done to diagnose a new patient with an autoimmune disease.


Photos: https://www.ncbi.nlm.nih.gov/pubmed/16126512

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