Abstract
Although there are plausible and attractive laboratory data supporting an etiologic role for YE infections in the initiation of autoimmune thyroid diseases (AITD), the epidemiological data are far less convincing. The original hypothesis of cross-reactivity between the TSH-R and Yersinia Enterocolitica (YE) would suggest a link only with GD. However, most studies find a similar prevalence of YE antibodies in Graves' disease (GD) and HT patients. Also, if YE infections are one of the environmental risk factors for AITD, the prevalence figures for YE are rather puzzling. First, acute gastro-enteritis caused by YE is rare in comparison with the incidence of AITD. Secondly, if not acute but chronic persisting YE infections are the culprit, there prevalence in controls is surprisingly high—ranging from 17.5 till >90%. In the Amsterdam cohort of healthy female relatives of AITD patients, positive YE serology was not linked to thyroid autoimmunity, but the prevalence of YE antibodies was yet higher than in controls. One hypothesis to explain this is that these relatives shared a genetic background with an increased susceptibility for chronic, persistent YE infection. This is supported by the observation that not all rat strains infected with YE develop a chronic persistent infection. In some strains, the anti Yersinia outermembrane proteins (YOP) antibodies disappeared when the infection was cleared, while in others, antibodies and infection persisted. Therefore, there is a possibility that a continuous stimulation of the immune system from YE infected plaques of Peyer in susceptible humans stimulates thyroid autoimmunity.
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