| First Author | Petermann F | Year | 2010 |
| Journal | Immunity | Volume | 33 |
| Issue | 3 | Pages | 351-63 |
| PubMed ID | 20832339 | Mgi Jnum | J:164420 |
| Mgi Id | MGI:4833879 | Doi | 10.1016/j.immuni.2010.08.013 |
| Citation | Petermann F, et al. (2010) gammadelta T cells enhance autoimmunity by restraining regulatory T cell responses via an interleukin-23-dependent mechanism. Immunity 33(3):351-63 |
| abstractText | Mice that lack interleukin-23 (IL-23) are resistant to T cell-mediated autoimmunity. Although IL-23 is a maturation factor for T helper 17 (Th17) cells, a subset of gammadelta T cells expresses the IL-23 receptor (IL-23R) constitutively. Using IL-23R reporter mice, we showed that gammadelta T cells were the first cells to respond to IL-23 during experimental autoimmune encephalomyelitis (EAE). Although gammadelta T cells produced Th17 cell-associated cytokines in response to IL-23, their major function was to prevent the development of regulatory T (Treg) cell responses. IL-23-activated gammadelta T cells rendered alphabeta effector T cells refractory to the suppressive activity of Treg cells and also prevented the conversion of conventional T cells into Foxp3(+) Treg cells in vivo. Thus, IL-23, which by itself has no direct effect on Treg cells, is able to disarm Treg cell responses and promote antigen-specific effector T cell responses via activating gammadelta T cells. |
