The activation and regulation of IL-17 receptor mediated signaling

Cytokine. 2013 May;62(2):175-82. doi: 10.1016/j.cyto.2013.03.014. Epub 2013 Apr 1.

Abstract

Interleukin-17 (IL-17), the signature cytokine produced by T helper 17 (Th17) cells, plays pivotal roles in host defense responses against microbial invasion, as well as in the pathogenesis of autoimmune diseases and allergic syndromes. IL-17 activates several downstream signaling pathways including NF-κB, MAPKs and C/EBPs to induce gene expression of antibacterial peptides, proinflammatory chemokines and cytokines and matrix metalloproteinases (MMPs). IL-17 can also stabilize mRNAs of genes induced by TNFα. Although the physiological and pathological functions of IL-17 have been studied for many years, the landscape of its signaling transduction has not been described until recently. The cytosolic adaptor molecule Act1 (also known as CIKS) is considered as the master mediator of IL-17 signaling. In this review, we will summarize recent progress on activation and regulation of IL-17 mediated signal transduction, especially on Act1 mediated regulation of the signaling.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Autoimmune Diseases / immunology
  • CCAAT-Enhancer-Binding Proteins / metabolism
  • Humans
  • Interleukin-17 / immunology
  • Interleukin-17 / metabolism*
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / metabolism
  • Receptors, Interleukin-17 / immunology
  • Receptors, Interleukin-17 / metabolism*
  • Signal Transduction
  • Th17 Cells / metabolism*
  • Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • CCAAT-Enhancer-Binding Proteins
  • Interleukin-17
  • NF-kappa B
  • Receptors, Interleukin-17
  • TRAF3IP2 protein, human
  • Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
  • Tumor Necrosis Factor-alpha
  • Mitogen-Activated Protein Kinases