Environment and Autoimmunity: Facts and Gaps
Autoimmune diseases are comprehensive models of complex conditions in which an individual’s genetic susceptibility is necessary but not sufficient to explain disease onset, perpetuation, and severity. This is well represented by the variable but invariably incomplete concordance rates for all autoimmune diseases in monozygotic twins. In the broad group of autoimmune diseases, heritability ranges between 0.008 and 1 with median values of approximately 0.60. A complementary term coined “environmentability” may well represent the environmental influence on the individual phenotype and can include dietary habits, chemicals, or hygienic conditions via several molecular and epigenetic mechanisms. Numerous environmental factors have been proposed for systemic and organ-specific autoimmune diseases. The National Institute of Environmental Health Sciences (NIEHS) convened an expert panel workshop to review the body of literature examining the role of the environment in the development of autoimmune disease and to identify conclusions, certainties, and critical knowledge gaps in this area. The results of the workshop and the literature illustrate that several kinds of epidemiological, mechanistic, and model evidence support specific chemical and physical factors as well as infectious agents.
KeywordsSystemic Lupus Erythematosus Autoimmune Disease Rheumatic Fever Aryl Hydrocarbon Receptor Nicotine Pretreatment
- Miller FW, Alfredsson L, Costenbader KH, Kamen DL, Nelson LM, Norris JM, De Roos AJ (2012a) Epidemiology of environmental exposures and human autoimmune diseases: findings from a National Institute of Environmental Health Sciences Expert Panel Workshop. J Autoimmun 39:259–271PubMedCentralCrossRefPubMedGoogle Scholar
- Nistico L, Fagnani C, Coto I, Percopo S, Cotichini R, Limongelli MG, Paparo F, D’Alfonso S, Giordano M, Sferlazzas C, Magazzu G, Momigliano-Richiardi P, Greco L, Stazi MA (2006) Concordance, disease progression, and heritability of coeliac disease in Italian twins. Gut 55:803–808PubMedCentralCrossRefPubMedGoogle Scholar
- van der Woude D, Houwing-Duistermaat JJ, Toes RE, Huizinga TW, Thomson W, Worthington J, van der Helm-van Mil AH, de Vries RR (2009) Quantitative heritability of anti-citrullinated protein antibody-positive and anti-citrullinated protein antibody-negative rheumatoid arthritis. Arthritis Rheum 60:916–923CrossRefPubMedGoogle Scholar