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Publication Detail
Mice lacking endogenous IL-10-producing regulatory B cells develop exacerbated disease and present with an increased frequency of Th1/Th17 but a decrease in regulatory T cells.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Carter NA, Vasconcellos R, Rosser EC, Tulone C, Muñoz-Suano A, Kamanaka M, Ehrenstein MR, Flavell RA, Mauri C
  • Publication date:
    15/05/2011
  • Pagination:
    5569, 5579
  • Journal:
    J Immunol
  • Volume:
    186
  • Issue:
    10
  • Status:
    Published
  • Country:
    United States
  • PII:
    jimmunol.1100284
  • Language:
    eng
  • Keywords:
    Adoptive Transfer, Animals, Arthritis, Autoimmunity, B-Lymphocyte Subsets, CD4 Antigens, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Forkhead Transcription Factors, Inflammation, Interferon-gamma, Interleukin-10, Interleukin-17, Interleukin-2 Receptor alpha Subunit, Mice, Mice, Inbred C57BL, Mice, Transgenic, Precursor Cells, B-Lymphoid, T-Lymphocytes, Regulatory, Th1 Cells, Th17 Cells
Abstract
IL-10-producing B cells, also known as regulatory B cells (Bregs), play a key role in controlling autoimmunity. In this study, we report that chimeric mice specifically lacking IL-10-producing B cells (IL-10(-/-)B cell) developed an exacerbated arthritis compared with chimeric wild-type (WT) B cell mice. A significant decrease in the absolute numbers of Foxp3 regulatory T cells (Tregs), in their expression level of Foxp3, and a marked increase in inflammatory Th1 and Th17 cells were detected in IL-10(-/-) B cell mice compared with WT B cell mice. Reconstitution of arthritic B cell deficient (μMT) mice with different B cell subsets revealed that the ability to modulate Treg frequencies in vivo is exclusively restricted to transitional 2 marginal zone precursor Bregs. Moreover, transfer of WT transitional 2 marginal zone precursor Bregs to arthritic IL-10(-/-) mice increased Foxp3(+) Tregs and reduced Th1 and Th17 cell frequencies to levels measured in arthritic WT mice and inhibited inflammation. In vitro, IL-10(+/+) B cells established longer contact times with arthritogenic CD4(+)CD25(-) T cells compared with IL-10(-/-) B cells in response to Ag stimulation, and using the same culture conditions, we observed upregulation of Foxp3 on CD4(+) T cells. Thus, IL-10-producing B cells restrain inflammation by promoting differentiation of immunoregulatory over proinflammatory T cells.
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