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Trends Immunol. 2011 May;32(5):232-9. doi: 10.1016/j.it.2011.02.007. Epub 2011 Apr 12.

IL-17 receptor signaling and T helper 17-mediated autoimmune demyelinating disease.

Author information

1
Department of Immunology, Cleveland Clinic Cleveland, OH 44195, USA.

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.

PMID:
21493143
PMCID:
PMC3329781
DOI:
10.1016/j.it.2011.02.007
[Indexed for MEDLINE]
Free PMC Article

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