Synovial fluid‐derived Yersinia‐reactive T cells responding to human 65‐kDa heat‐shock protein and heat‐stressed antigen‐presenting cells

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Abstract
Humoral and cellular immune reactions to heat‐shock proteins have been implicated in the pathogenesis of arthritis. Heat‐shock proteins occur in bacteria as well as all eukaryotes and have been highly conserved during evolution. Cross‐reactivity between bacterial and human heat‐shock proteins induced at the site of inflammation may underlie the pathogenesis of some forms of arthritis. In order to test this hypothesis, we raised and cloned a Yersinia‐specific T cell line from the synovial fluid lymphocytes of a patient with Yesinia‐induced reactive arthritis. From this line we obtained a CD4+ T cell clone that proliferated in response to Yersinia antigens and both to the mycobacterial and the human 65‐kDa heat‐shock protein. This T cell clone also proliferated in response to autologous heat‐stressed antigen‐presenting cells as well as to synovial fluid mononuclear cells from the inflamed joint, thus showing true autoreactivity against endogenously synthetized self‐antigen. These results demonstrate the induction of an autoimmune T cell response by a natural bacterial infection and support the important role of heat‐shock proteins in the pathogenesis of immune‐mediated arthritis.