title: Synovial fluid MHC-unrestricted gamma delta-T lymphocytes contribute to antibacterial and anti-self cytotoxicity in the spondylarthropathies.
abstract: OBJECTIVE
  In reactive arthritis (ReA), synovial fluid-derived bacteria-specific CD4+ and CD8+ T cells have been studied intensively in recent years. We have addressed the question whether gamma delta-TCR+ lymphocytes could contribute to antibacterial or anti-self cytotoxicity in the affected joints of patients, with spondylarthropathies.
  
  
  METHODS
  T cell clones were derived by random cloning from the synovial fluids of one patient with Yersinia-induced ReA, one patient with a Yersinia-induced flare up of pre-existing ankylosing spondylitis, and one patient with ankylosing spondylitis. Eight clones with a CD3+, alpha beta-TCR-, CD4-, CD8- and gamma delta-TCR+ phenotype (all expressing V gamma 9) were tested in a standard 52Cr-release assay using autologous or allogeneic B cell lines, CIR-B27, Daudi cells, and RJ.225 cells.
  
  
  RESULTS
  Four gamma delta-TCR+ clones killed both autologous and allogeneic target cells when infected with live Yersinia or Salmonella and also uninfected Daudi cells expressing GroEL heatshock protein. One clone was specific for Yersinia-infected targets. Three gamma delta-TCR+ clones were cytotoxic when uninfected autologous or allogeneic targets were employed. Polymorphic "classical" MHC class I or class II molecules were not used as restriction elements.
  
  
  CONCLUSIONS
  We conclude that, upon in vivo contact with bacteria such as Yersinia and Salmonella, synovial gamma delta-T lymphocytes are activated and contribute to antibacterial immunity via specific target cell lysis. Furthermore, anti-self cytolytic gamma delta-T cells could participate in the clearance of stressed and detrimental cells in the arthritic joint or, alternatively, could support the chronicity of autoimmune arthritis.
authors.affiliation: First Department of Internal Medicine, Johannes Gutenberg-University of Mainz, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Hermann
authors.forename: B
authors.initials: B
authors.lastname: Ackermann
authors.forename: R
authors.initials: R
authors.lastname: Duchmann
authors.forename: K H
authors.initials: KH
authors.lastname: Meyer zum Büschenfelde
mesh_terms: D000328:Adult; D016918:Arthritis, Reactive / Q000209:etiology / Q000276:immunology; D015551:Autoimmunity; D001419:Bacteria / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D006801:Humans; D066298:In Vitro Techniques; D007592:Joint Diseases / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D000091402:Prohibitins; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism*; D012475:Salmonella / Q000276:immunology; D013122:Spinal Diseases / Q000276:immunology*; D013167:Spondylitis, Ankylosing / Q000276:immunology; D013582:Synovial Fluid / Q000166:cytology / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D015007:Yersinia / Q000276:immunology; D015009:Yersinia Infections / Q000150:complications
chemical_list: C000717331:PHB2 protein, human; D000091402:Prohibitins; D016692:Receptors, Antigen, T-Cell, gamma-delta