Abstract
Genetic composition and major histocompatibility complex polymorphisms unequivocally predispose to autoimmune disease, but environmental factors also play a critical role in precipitating disease in susceptible individuals. Notorious among these has been microbial infection. Older studies describing associations between microbial infection and autoimmune disease are now followed by new studies demonstrating correlations between susceptibility to autoimmune disease and commensal colonization of the intestinal tract. T helper 17 (T(H)17) cells have gained a prominent role in autoimmune disease, and notably, their development within the intestine has been linked to colonization with specific commensal bacteria. Here, we consider current views on how microbes, T(H)17 cells, and autoimmunity are connected. We speculate on how the intricate relationships among commensal, pathogen, and the host might ultimately determine susceptibility to autoimmune disease.