| First Author | Sheng JR | Year | 2015 |
| Journal | J Neuroimmunol | Volume | 289 |
| Pages | 130-8 | PubMed ID | 26616882 |
| Mgi Jnum | J:330977 | Mgi Id | MGI:6869041 |
| Doi | 10.1016/j.jneuroim.2015.10.023 | Citation | Sheng JR, et al. (2015) IL-10 derived from CD1dhiCD5(+) B cells regulates experimental autoimmune myasthenia gravis. J Neuroimmunol 289:130-8 |
| abstractText | IL-10-competent subset within CD1d(hi)CD5(+) B cells, also known as B10 cells, has been shown to regulate autoimmune diseases. In our previous study, adoptive transfer of CD1d(hi)CD5(+) 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 CD1d(hi)CD5(+) B cells sorted from WT mice, but not IL-10 deficient CD1d(hi)CD5(+) B cells exhibited regulatory function in vitro and in vivo. Adoptive transfer of IL-10 competent CD1d(hi)CD5(+) 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 CD1d(hi)CD5(+) B cells plays an important role in immune regulation of EAMG. |
