The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17–producing effector T helper cells in vivo

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Abstract
Whether interleukin 23 (IL-23) affects the differentiation of or simply the maintenance of IL-17–producing helper T cells (TH-17 cells) is unclear. Cua and colleagues show that IL-23 is required for the full differentiation and proliferation of effector TH-17 cells in vivo. Interleukin 23 (IL-23) is required for autoimmune inflammation mediated by IL-17-producing helper T cells (TH-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 TH-17 cells in autoimmunity, inflammation and infection. In the absence of IL-23, TH-17 development was stalled at the early activation stage. TH-17 cells failed to downregulate IL-2 and also failed to maintain IL-17 production or upregulate expression of the IL-7 receptor α-chain. These defects were associated with less proliferation; consequently, fewer effector TH-17 cells were produced in the lymph nodes and hence available to emigrate to the bloodstream and tissues.