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Publication Detail
B cell resistance to Fas-mediated apoptosis contributes to their ineffective control by regulatory T cells in rheumatoid arthritis.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Rapetti L, Chavele K-M, Evans CM, Ehrenstein MR
  • Publication date:
  • Pagination:
    294, 302
  • Journal:
    Ann Rheum Dis
  • Volume:
  • Issue:
  • Status:
  • Country:
  • PII:
  • Language:
  • Keywords:
    Autoimmunity, B cells, Rheumatoid Arthritis, T Cells, Apoptosis, Arthritis, Rheumatoid, B-Lymphocytes, Case-Control Studies, Female, Flow Cytometry, Humans, Leukocytes, Mononuclear, Lymphocyte Activation, Male, T-Lymphocytes, Regulatory, fas Receptor
OBJECTIVE: To investigate whether regulatory T cells (Treg) can control B cell function in rheumatoid arthritis (RA) and if not to explore the basis for this defect. METHODS: Suppression of B cell responses by Treg was analysed in vitro by flow cytometry and ELISA using peripheral blood mononuclear cells from 65 patients with RA and 41 sex-matched and aged-matched healthy volunteers. Blocking and agonistic antibodies were used to define the role of Fas-mediated apoptosis in B cell regulation. RESULTS: Treg failed to restrain B cell activation, proinflammatory cytokine and antibody production in the presence of responder T cells in RA patients. This lack of suppression was not only caused by impaired Treg function but was also due to B cell resistance to regulation. In healthy donors, control by Treg was associated with increased B cell death and relied upon Fas-mediated apoptosis. In contrast, RA B cells had reduced Fas expression compared with their healthy counterparts and were resistant to Fas-mediated apoptosis. CONCLUSIONS: These studies demonstrate that Treg are unable to limit B cell responses in RA. This appears to be primarily due to B cell resistance to suppression, but Treg defects also contribute to this failure of regulation. Our data identify the Fas pathway as a novel target for Treg-mediated suppression of B cells and highlight a potential therapeutic approach to restore control of B cells by Treg in RA patients.
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