HUMAN GAMMA-DELTA T-CELL RECOGNITION OF YERSINIA-ENTEROCOLITICA

We have studied the human gamma delta T-cell response to Yersinia ente rocolitica, a facultative intracellular bacterium which causes gastroe nteritis and, particularly in human leucocyte antigen (HLA)-B27(+) ind ividuals, reactive arthritis (ReA). A marked proliferation of that cyt otoxic gamma delta T cells is seen when Yersinia-infected lymphoblasto id cell lines or fixed intact Yersinia are added to cultures of mononu clear cells derived from the synovial fluid of ReA patients or from th e peripheral blood of healthy donors. In contrast, heat-inactivated Ye rsinia fail to stimulate the gamma delta T-cell response. The gamma de lta T-cell lines generated killed both autologous and allogeneic infec ted cell lines. Interestingly, a T-cell line generated from synovial f luid mononuclear cells (SFMC) killed infected autologous cell lines an d a cell line matched for HLA-B27 less well than infected allogeneic t arget cells. gamma delta T-cell clones isolated from this line were fo und to express V gamma 9V delta 2 T-cell receptor (TCR) and also kille d infected mismatched cells more efficiently than autologous targets. Moreover, from experiments using major histocompatability complex (MHC )-deficient cell lines, it was apparent that target cell recognition w as MHC independent. Our results suggest that gamma delta T cells can b e involved in immunity to Yersinia enterocolitica and should be taken into account when considering immunopathological mechanisms leading to reactive arthritis.