| First Author | Cai G | Year | 2012 |
| Journal | J Immunol | Volume | 189 |
| Issue | 3 | Pages | 1294-302 |
| PubMed ID | 22753938 | Mgi Jnum | J:189772 |
| Mgi Id | MGI:5446978 | Doi | 10.4049/jimmunol.1102948 |
| Citation | Cai G, et al. (2012) A regulatory role for IL-10 receptor signaling in development and B cell help of T follicular helper cells in mice. J Immunol 189(3):1294-302 |
| abstractText | IL -10 is widely accepted as a survival, proliferation, and differentiation factor for B cells. However, IL-10 deficiency accelerates disease progression as the result of autoantibody production in many autoimmune disease models. It was demonstrated that T follicular helper cells (T(FH) cells) play a key role in helping B cells that are secreting Abs. In this study, we demonstrated a regulatory role for IL-10R signaling on the development and B cell help function of T(FH) cells in vitro and in vivo. IL-1R subunit beta-deficient (Il10rb(-/-)) Th cells were able to differentiate more readily into T(FH) cells, as well as secrete more IL-21 and IL-17 compared with wild-type Th cell-derived T(FH) cells. Increased IL-21 and IL-17 contributed to the enhanced B cell help functions of T(FH) cells. Further experiments demonstrated that IL-6 and IL-23 from dendritic cells in Il10rb(-/-) mice contributed to the differentiation of naive Th cells into T(FH) cells, as well as the generation of IL-21- and IL-17-producing T(FH) cells. Our results provide useful information for clarifying the immunoregulatory mechanisms associated with IL-10 deficiency in certain autoimmune disease models. This information could also be of benefit for the development of vaccines. |
