title: IL-17 receptor signaling and T helper 17-mediated autoimmune demyelinating disease.
abstract: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is widely used to dissect molecular mechanisms of MS and to develop new therapeutic strategies. The T helper 17 (Th17) subset of CD4 T cells plays a crucial role in the development of EAE. IL-17, a cytokine produced by Th17 cells, participates in EAE pathogenesis through induction of inflammatory gene expression in target cells. Recent work has shown that Act1, a U-box E3 ubiquitin ligase, is recruited to IL-17 receptor (IL-17R) upon IL-17 stimulation and is required for IL-17-mediated signaling. Here, we review the molecular and cellular mechanisms by which IL-17 and Act1-mediated signaling contribute to EAE.
authors.affiliation: Department of Immunology, Cleveland Clinic Cleveland, OH 44195, USA.
authors.forename: Jarod
authors.initials: J
authors.lastname: Zepp
authors.forename: Ling
authors.initials: L
authors.lastname: Wu
authors.forename: Xiaoxia
authors.initials: X
authors.lastname: Li
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology; D003711:Demyelinating Diseases / Q000276:immunology / Q000473:pathology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000473:pathology; D006801:Humans; D051379:Mice; D009103:Multiple Sclerosis / Q000276:immunology / Q000473:pathology; D053722:Receptors, Interleukin-17 / Q000378:metabolism*; D015398:Signal Transduction; D058504:Th17 Cells / Q000276:immunology*; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / Q000378:metabolism
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D053722:Receptors, Interleukin-17; C414202:TRAF3IP2 protein, human; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins