IFN-β treatment requires B cells for efficacy in neuroautoimmunity.

نویسندگان

  • Ryan D Schubert
  • Yang Hu
  • Gaurav Kumar
  • Spencer Szeto
  • Peter Abraham
  • Johannes Winderl
  • Joel M Guthridge
  • Gabriel Pardo
  • Jeffrey Dunn
  • Lawrence Steinman
  • Robert C Axtell
چکیده

IFN-β remains the most widely prescribed treatment for relapsing remitting multiple sclerosis. Despite widespread use of IFN-β, the therapeutic mechanism is still partially understood. Particularly, the clinical relevance of increased B cell activity during IFN-β treatment is unclear. In this article, we show that IFN-β pushes some B cells into a transitional, regulatory population that is a critical mechanism for therapy. IFN-β treatment increases the absolute number of regulatory CD19(+)CD24(++)CD38(++) transitional B cells in peripheral blood relative to treatment-naive and Copaxone-treated patients. In addition, we found that transitional B cells from both healthy controls and IFN-β-treated MS patients are potent producers of IL-10, and that the capability of IFN-β to induce IL-10 is amplified when B cells are stimulated. Similar changes are seen in mice with experimental autoimmune encephalomyelitis. IFN-β treatment increases transitional and regulatory B cell populations, as well as IL-10 secretion in the spleen. Furthermore, we found that IFN-β increases autoantibody production, implicating humoral immune activation in B cell regulatory responses. Finally, we demonstrate that IFN-β therapy requires immune-regulatory B cells by showing that B cell-deficient mice do not benefit clinically or histopathologically from IFN-β treatment. These results have significant implications for the diagnosis and treatment of relapsing remitting multiple sclerosis.

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عنوان ژورنال:
  • Journal of immunology

دوره 194 5  شماره 

صفحات  -

تاریخ انتشار 2015