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Publication Detail
CD19+CD24hiCD38hi B cells maintain regulatory T cells while limiting TH1 and TH17 differentiation.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Flores-Borja F, Bosma A, Ng D, Reddy V, Ehrenstein MR, Isenberg DA, Mauri C
  • Publication date:
    20/02/2013
  • Pagination:
    173ra23, ?
  • Journal:
    Sci Transl Med
  • Volume:
    5
  • Issue:
    173
  • Status:
    Published
  • Country:
    United States
  • PII:
    5/173/173ra23
  • Language:
    eng
  • Keywords:
    ADP-ribosyl Cyclase 1, Adult, Aged, Aged, 80 and over, Antigens, CD19, Arthritis, Rheumatoid, B-Lymphocytes, CD24 Antigen, Cell Differentiation, Female, Humans, Interferon-gamma, Interleukin-6, Interleukin-8, Male, Middle Aged, T-Lymphocytes, Regulatory, Tumor Necrosis Factor-alpha, Young Adult
Abstract
The relevance of regulatory B cells in the maintenance of tolerance in healthy individuals or in patients with immune disorders remains understudied. In healthy individuals, CD19(+)CD24(hi)CD38(hi) B cells suppress CD4(+)CD25(-) T cell proliferation as well as the release of interferon-γ and tumor necrosis factor-α by these cells; this suppression is partially mediated through the production of interleukin-10 (IL-10). We further elucidate the mechanisms of suppression by CD19(+)CD24(hi)CD38(hi) B cells. Healthy CD19(+)CD24(hi)CD38(hi) B cells inhibited naïve T cell differentiation into T helper 1 (T(H)1) and T(H)17 cells and converted CD4(+)CD25(-) T cells into regulatory T cells (T(regs)), in part through the production of IL-10. In contrast, CD19(+)CD24(hi)CD38(hi) B cells from patients with rheumatoid arthritis (RA) failed to convert CD4(+)CD25(-) T cells into functionally suppressive T(regs) or to curb T(H)17 development; however, they maintained the capacity to inhibit T(H)1 cell differentiation. Moreover, RA patients with active disease have reduced numbers of CD19(+)CD24(hi)CD38(hi) B cells in peripheral blood compared with either patients with inactive disease or healthy individuals. These results suggest that in patients with active RA, CD19(+)CD24(hi)CD38(hi) B cells with regulatory function may fail to prevent the development of autoreactive responses and inflammation, leading to autoimmunity.
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