Yersinia enterocolitica O:3 and the human thyrotropin receptor share a structural similarity, revealed by their serological cross-reactivity. The exact molecular basis of the similarity is open. In spite of this cross-reactivity, Yersinia seems not to be a major inducer of thyroid autoimmunity. Yersinia infections or avirulent Yersinia strains in the intestinal flora may rather contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals. Regarding Yersinia and spondyloarthropathies, it is undetermined whether the chronic sequelae of acute Yersinia-triggered reactive arthritis are due to the persistence of phlogistic microbial components or to autoimmunity, or to both. No convincing evidence exists for a role of molecular mimicry between Yersinia and HLA B27 or other host structures. Cytotoxic T-cell clones derived from synovial fluid, and capable of killing Yersinia-infected and uninfected autologous targets in an HLA B27-restricted fashion have recently been described. Evaluation of their significance for the potential Yersinia-induced autoimmunity is waiting for characterization of the bacterial and host peptides involved.

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