| First Author | Ahern PP | Year | 2010 |
| Journal | Immunity | Volume | 33 |
| Issue | 2 | Pages | 279-88 |
| PubMed ID | 20732640 | Mgi Jnum | J:163906 |
| Mgi Id | MGI:4830178 | Doi | 10.1016/j.immuni.2010.08.010 |
| Citation | Ahern PP, et al. (2010) Interleukin-23 drives intestinal inflammation through direct activity on T cells. Immunity 33(2):279-88 |
| abstractText | Mutations in the IL23R gene are linked to inflammatory bowel disease susceptibility. Experimental models have shown that interleukin-23 (IL-23) orchestrates innate and T cell-dependent colitis; however, the cell populations it acts on to induce intestinal immune pathology are unknown. Here, using Il23r(-/-) T cells, we demonstrated that T cell reactivity to IL-23 was critical for development of intestinal pathology, but not for systemic inflammation. Through direct signaling into T cells, IL-23 drove intestinal T cell proliferation, promoted intestinal Th17 cell accumulation, and enhanced the emergence of an IL-17A(+)IFN-gamma(+) population of T cells. Furthermore, IL-23R signaling in intestinal T cells suppressed the differentiation of Foxp3(+) cells and T cell IL-10 production. Although Il23r(-/-) T cells displayed unimpaired Th1 cell differentiation, these cells showed impaired proliferation and failed to accumulate in the intestine. Together, these results highlight the multiple functions of IL-23 signaling in T cells that contribute to its colitogenic activity. |
