Context: Autoimmune thyroid disease (AITD) is the archetypal organ-specific autoimmune disorder and is characterized by the production of thyroid autoantibodies. However, the underlying mechanisms by which specific antibodies against thyroid proteins are produced are largely unknown.
Evidence acquisition: Published peer-reviewed basic and clinical literatures on immunology and autoimmune diseases were identified through searches of PubMed for articles published from January 1971 to May 2011. Articles resulting from these searches and relevant references cited in those articles were reviewed. All the relevant articles were written in English.
Evidence synthesis: Recent studies have indicated that innate immune responses induced by both exogenous and endogenous factors affect the phenotype and severity of autoimmune reactions. One of the recent topics is the effect of self-genomic DNA fragments on immune activation. Expression of major histocompatibility complex class II on the autoimmune target cells seems to play an important role in the presentation of endogenous antigens. Accumulated evidence from animal models has generated new insights into the pathogenesis of AITD.
Conclusion: AITD develops by a combination of genetic susceptibility and environmental factors. Innate immune responses are associated with thyroid dysfunction, tissue destruction, and the likely development and perpetuation of AITD. In addition to the other factors, cell injury may contribute to the activation of innate immune response and the development of AITD.