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Epistasis and immunity: the role of genetic interactions in autoimmune diseases
Author(s) -
Rose Anna M.,
Bell Lucy C. K.
Publication year - 2012
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2012.03623.x
Subject(s) - epistasis , autoimmunity , immunology , autoimmune disease , biology , immune system , rheumatoid arthritis , genetics , systemic lupus erythematosus , gene , disease , medicine , antibody
Summary Autoimmune disorders are a complex and varied group of diseases that are caused by breakdown of self‐tolerance. The aetiology of autoimmunity is multi‐factorial, with both environmental triggers and genetically determined risk factors. In recent years, it has been increasingly recognized that genetic risk factors do not act in isolation, but rather the combination of individual additive effects, gene–gene interactions and gene–environment interactions determine overall risk of autoimmunity. The importance of gene–gene interactions, or epistasis, has been recently brought into focus, with research demonstrating that many autoimmune diseases, including rheumatic arthritis, autoimmune glomerulonephritis, systemic lupus erythematosus and multiple sclerosis, are influenced by epistatic interactions. This review sets out to examine the basic mechanisms of epistasis, how epistasis influences the immune system and the role of epistasis in two major autoimmune conditions, systemic lupus erythematosus and multiple sclerosis.