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Publication Detail
Interleukin-10 produced by B cells is crucial for the suppression of Th17/Th1 responses, induction of T regulatory type 1 cells and reduction of collagen-induced arthritis.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Carter NA, Rosser EC, Mauri C
  • Publication date:
    08/02/2012
  • Pagination:
    R32, ?
  • Journal:
    Arthritis Res Ther
  • Volume:
    14
  • Issue:
    1
  • Status:
    Published online
  • Country:
    England
  • PII:
    ar3736
  • Language:
    eng
  • Keywords:
    Animals, Arthritis, Experimental, B-Lymphocytes, Cell Differentiation, Cell Proliferation, Disease Progression, Female, Flow Cytometry, Forkhead Transcription Factors, Interferon-gamma, Interleukin-10, Interleukin-17, Male, Mice, Mice, Inbred DBA, Mice, Knockout, T-Lymphocytes, Regulatory, Th1 Cells, Th17 Cells
Abstract
INTRODUCTION: Interleukin-10 (IL-10) producing B cells, also known as regulatory B (Breg) cells, play a key role in controlling autoimmunity. Our laboratory and others have demonstrated a pivotal role for Bregs in rheumatological disorders, including experimental models of arthritis and lupus. The aim of this study was to identify the role of endogenous IL-10 secreting B cells in vivo in controlling the induction and disease progression of collagen-induced arthritis (CIA). METHODS: We generated chimeric mice that had IL-10 knocked-out specifically in the B cell population. These mice were compared with wild-type (WT) B cell chimeric mice for their susceptibility to CIA. RESULTS: Here we report that chimeric mice specifically lacking IL-10 producing B cells (IL-10-/- B cell) developed an exacerbated CIA compared to chimeric wild type B cell (WT B cell) mice. A marked increase in inflammatory Th1 and Th17 cells were detected in IL-10-/-B cell mice compared to WT B cell mice. Furthermore, there was a reduction in IL-10 secreting CD4+ Tr1 cells in these animals. CONCLUSIONS: IL-10 producing B cells restrain inflammation by promoting differentiation of immuno-regulatory over pro-inflammatory T cells and, hence, act to maintain tolerance.
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Inflammation
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