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

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


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.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Autoimmune Diseases* / immunology
  • Autoimmune Diseases* / pathology
  • Demyelinating Diseases* / immunology
  • Demyelinating Diseases* / pathology
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Encephalomyelitis, Autoimmune, Experimental / pathology
  • Humans
  • Mice
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / pathology
  • Receptors, Interleukin-17 / metabolism*
  • Signal Transduction*
  • Th17 Cells / immunology*
  • Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / metabolism


  • Adaptor Proteins, Signal Transducing
  • Receptors, Interleukin-17
  • TRAF3IP2 protein, human
  • Tumor Necrosis Factor Receptor-Associated Peptides and Proteins