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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?
Author(s) -
Birgit Ackermann,
Martin S. Staege,
Angelika B. ReskeKunz,
HansPeter Dienes,
KarlHermann Meyer zum Büschenfelde,
E. MärkerHermann
Publication year - 1997
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/516451
Subject(s) - cytotoxic t cell , antigen , immune system , immunology , antigen presenting cell , biology , ctl* , reactive arthritis , microbiology and biotechnology , cd8 , t cell , antigen presentation , t lymphocyte , yersinia , arthritis , bacteria , in vitro , biochemistry , genetics
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.

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