Infection, thyroid disease, and autoimmunity

Traditionally, it was assumed that infectious agents induced disease by causing direct tissue damage (for example via secretion of exotoxins and endotoxins). However, we now know only too well that infectious agents play a role in the induction of noninfectious consequences, including malignancies (for example Ebstein Barr virus and Burkitt’s lymphoma, HTLV-1, and adult T cell leukemia), acquired immunodeficiency syndrome (human immunodeficiency virus), peptic ulcer (Helicobacter pylori), and autoimmune diseases. Infectious agents have been implicated in the pathogenesis of a variety of autoimmune diatheses, namely, rheumatic fever, Reiter’s syndrome, systemic lupus erythematosus (SLE), myasthenia gravis, insulin-dependent diabetes mellitus, Sjogren’s syndrome, and the autoimmune thyroid diseases. This review examines the pertinent data relating to the possible role of infecting organisms in the development of autoimmune thyroid diseases (AITD), with an emphasis on human disease, focusing on the mechanisms by which infection could trigger Graves’ disease and other thyroiditides. It must be remembered, however, that the role of infection in precipitating human AITD remains purely hypothetical and that precipitating factors may not be either infectious or external.