| First Author | McGeachy MJ | Year | 2009 |
| Journal | Nat Immunol | Volume | 10 |
| Issue | 3 | Pages | 314-24 |
| PubMed ID | 19182808 | Mgi Jnum | J:146856 |
| Mgi Id | MGI:3838684 | Doi | 10.1038/ni.1698 |
| Citation | McGeachy MJ, et al. (2009) The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo. Nat Immunol 10(3):314-24 |
| abstractText | Interleukin 23 (IL-23) is required for autoimmune inflammation mediated by IL-17-producing helper T cells (T(H)-17 cells) and has been linked to many human immune disorders. Here we restricted deficiency in the IL-23 receptor to defined cell populations in vivo to investigate the requirement for IL-23 signaling in the development and function of T(H)-17 cells in autoimmunity, inflammation and infection. In the absence of IL-23, T(H)-17 development was stalled at the early activation stage. T(H)-17 cells failed to downregulate IL-2 and also failed to maintain IL-17 production or upregulate expression of the IL-7 receptor alpha-chain. These defects were associated with less proliferation; consequently, fewer effector T(H)-17 cells were produced in the lymph nodes and hence available to emigrate to the bloodstream and tissues. |
