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

MJ McGeachy, Y Chen, CM Tato, A Laurence… - Nature …, 2009 - nature.com
MJ McGeachy, Y Chen, CM Tato, A Laurence, B Joyce-Shaikh, WM Blumenschein…
Nature immunology, 2009nature.com
Abstract 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 …
Abstract
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.
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