| First Author | Izcue A | Year | 2008 |
| Journal | Immunity | Volume | 28 |
| Issue | 4 | Pages | 559-70 |
| PubMed ID | 18400195 | Mgi Jnum | J:134507 |
| Mgi Id | MGI:3788989 | Doi | 10.1016/j.immuni.2008.02.019 |
| Citation | Izcue A, et al. (2008) Interleukin-23 restrains regulatory T cell activity to drive T cell-dependent colitis. Immunity 28(4):559-70 |
| abstractText | Interleukin-23 (IL-23) is an inflammatory cytokine that plays a key role in the pathogenesis of several autoimmune and inflammatory diseases. It orchestrates innate and T cell-mediated inflammatory pathways and can promote T helper 17 (Th17) cell responses. Utilizing a T cell transfer model, we showed that IL-23-dependent colitis did not require IL-17 secretion by T cells. Furthermore, IL-23-independent intestinal inflammation could develop if immunosuppressive pathways were reduced. The frequency of naive T cell-derived Foxp3+ cells in the colon increased in the absence of IL-23, indicating a role for IL-23 in controlling regulatory T cell induction. Foxp3-deficient T cells induced colitis when transferred into recipients lacking IL-23p19, showing that IL-23 was not essential for intestinal inflammation in the absence of Foxp3. Taken together, our data indicate that overriding immunosuppressive pathways is an important function of IL-23 in the intestine and could influence not only Th17 cell activity but also other types of immune responses. |
