IL-10 derived from CD1dhiCD5+ B cells regulates experimental autoimmune myasthenia gravis

•Bregs altered cytokine profile and inhibited anti-AChR Ab production via IL-10.•Adoptive transfer of IL-10 competent but not IL-10 deficient Bregs reduced the severity of disease in EAMG mice.•Adoptive transfer of IL-10 competent Bregs led to expansion of Tregs, IL-10+ T cells and Bregs.

IL-10-competent subset within CD1dhiCD5+ B cells, also known as B10 cells, has been shown to regulate autoimmune diseases. In our previous study, adoptive transfer of CD1dhiCD5+ B cells expanded in vivo by GM-CSF prevented and suppressed experimental autoimmune myasthenia gravis (EAMG). The goal of this study was to further examine the role and mechanism of IL-10 in the regulatory function of B10 cells in EAMG. We found that only IL-10 competent CD1dhiCD5+ B cells sorted from WT mice, but not IL-10 deficient CD1dhiCD5+ B cells exhibited regulatory function in vitro and in vivo. Adoptive transfer of IL-10 competent CD1dhiCD5+ B cells led to higher frequency of Tregs and B10 cells, and low levels of proinflammatory cytokines and autoantibody production. We conclude that IL-10 production within CD1dhiCD5+ B cells plays an important role in immune regulation of EAMG.

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