Enterobacteria-infected T cells as antigen-presenting cells for cytotoxic CD8 T cells: a contribution to the self-limitation of cellular immune reactions in reactive arthritis

In enterobacteria-induced reactive arthritis (ReA), different T cell subsets play a role in the induction and maintenance of the synovitic process. Synovial fluid–derived ab CD4, ab CD8, and gd T lymphocyte clones (TLC) that recognize Yersinia or Salmonella antigens on professional antigen-presenting cells (APC) have been characterized, and T cells themselves can function as nonprofessional APC. T cells were infected with the facultatively intracellular, arthritogenic entero-bacterium Yersinia enterocolitica O:3. A CD8 TLC isolated from a patient with Yersinia-induced ReA recognized and efficiently lysed autologous and allogeneic Yersinia-infected T cells. Infected cytotoxic T lymphocytes (CTL) had a reduced lytic capacity against syngeneic and allogeneic infected target cells, suggesting that the infection of CTL by bacteria may represent a mechanism of immune escape. In ReA, antigen presentation by T cells may modify the antibacterial immune response and may also contribute to network control mechanisms of T cell–mediated cytotoxicity. There is substantial interest in how T lymphocytes prevent [7]. However, the mechanisms by which the intraarticular im-or control infections with obligate or facultatively intracellular mune response to ‘‘arthritogenic’ ’ enterobacteria or, consecu-bacteria. In the case of reactive arthritides (ReA), which belong tively, to self-antigens is self-limited in the majority of patients to the so-called HLA-B27–associated spondylarthropathies, and chronic in others are not fully understood