McGeachy Mandy J, Chen Yi, Tato Cristina M, Laurence Arian, Joyce-Shaikh Barbara, Blumenschein Wendy M, McClanahan Terrill K, O'Shea John J, Cua Daniel J
Schering-Plough Biopharma, Palo Alto, California 94304, USA.
Nat Immunol. 2009 Mar;10(3):314-24. doi: 10.1038/ni.1698. Epub 2009 Feb 1.
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.
白细胞介素23（IL-23）是由产生IL-17的辅助性T细胞（T(H)-17细胞）介导的自身免疫炎症所必需的，并且与许多人类免疫疾病有关。在这里，我们在体内将IL-23受体的缺陷限制在特定的细胞群体中，以研究自身免疫、炎症和感染中T(H)-17细胞的发育和功能对IL-23信号传导的需求。在没有IL-23的情况下，T(H)-17细胞的发育在早期激活阶段停滞。T(H)-17细胞无法下调IL-2，也无法维持IL-17的产生或上调IL-7受体α链的表达。这些缺陷与增殖减少有关；因此，淋巴结中产生的效应T(H)-17细胞较少，从而可供迁移到血液和组织中。
