title: Interleukin-17C promotes Th17 cell responses and autoimmune disease via interleukin-17 receptor E.
abstract: Although several interleukin-17 (IL-17) family members and their receptors have been recently appreciated as important regulators in inflammatory diseases, the function of other IL-17 cytokines and IL-17 receptor-like molecules is unclear. Here we show that an IL-17 cytokine family member, IL-17C, was induced in a Th17 cell-dependent autoimmune disease and was required for its pathogenesis. IL-17C bound to IL-17RE, a member of IL-17 receptor family whose full-length isoform was selectively expressed in Th17 cells and signaled via an IL-17RA-RE receptor complex and the downstream adaptor Act1. IL-17C-IL-17RE induced the expression of a nuclear IkappaB family member, IκBζ, in Th17 cells to potentiate the Th17 cell response. Thus, our work has identified a cytokine-receptor pair with important function in regulating proinflammatory responses. This pathway may be targeted to treat autoimmune diseases.
authors: Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054-1901, USA.
authors: Seon Hee
authors: SH
authors: Chang
authors: Joseph M
authors: JM
authors: Reynolds
authors: Bhanu P
authors: BP
authors: Pappu
authors: Guangjie
authors: G
authors: Chen
authors: Gustavo J
authors: GJ
authors: Martinez
authors: Chen
authors: C
authors: Dong
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051550:I-kappa B Kinase / Q000378:metabolism; D020381:Interleukin-17 / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D053722:Receptors, Interleukin-17 / Q000172:deficiency / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction; D058504:Th17 Cells / Q000166:cytology / Q000276:immunology*
chemical_list: D020381:Interleukin-17; D053722:Receptors, Interleukin-17; D051550:I-kappa B Kinase