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RESEARCH PRODUCT

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?

Angelika B. Reske-kunzB. AckermannElisabeth Märker-hermannMartin S. StaegeHans-peter DienesKarl-hermann Meyer Zum Büschenfelde

subject

Salmonella typhimuriumYersinia InfectionsT cellT-LymphocytesAntigen presentationAntigen-Presenting Cellschemical and pharmacologic phenomenaBiologyArthritis ReactiveMicrobiologyInterleukin 21MiceL CellsAntigenT-Lymphocyte SubsetsProhibitinsmedicineTumor Cells CulturedImmunology and AllergyCytotoxic T cellAnimalsHumansIL-2 receptorAntigen-presenting cellYersinia enterocoliticaAntigens BacterialB-LymphocytesImmunity CellularNatural killer T cellClone CellsMicroscopy ElectronInfectious Diseasesmedicine.anatomical_structureImmunologybacteriaT-Lymphocytes Cytotoxic

description

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 alphabeta CD4, alphabeta CD8, and gammadelta 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 enterobacterium 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.

10.1086/516451https://pubmed.ncbi.nlm.nih.gov/9129075