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IL-17RC is required for IL-17A- and IL-17F-dependent signaling and the pathogenesis of experimental autoimmune encephalomyelitis.

It has been suggested that IL-17RC forms a complex with IL-17RA to mediate the functions of IL-17A and IL-17F homodimers as well as IL-17A/F heterodimers. It is still unclear whether IL-17RC is absolutely required for the signaling of IL-17 cytokines in vivo. By using Il-17rc-deficient mice, we show that IL-17RC is essential for the signaling of IL-17A, IL-17F, and IL-17A/F both in vitro and in vivo. IL-17RC does not preassociate with IL-17RA on the cell surface; rather IL-17A can induce the formation of an IL-17RC and IL-17RA complex. This process is not dependent on the intracellular similar expression to fibroblast growth factor genes and IL-17Rs (SEFIR) domain of IL-17RC, but the SEFIR is essential in IL-17A signal transduction. Finally, Il-17rc(-/-) mice develop much milder disease in an experimental autoimmune encephalomyelitis model, supporting an essential role for IL-17RC in mediating immune-mediated CNS inflammation.

Pubmed ID: 20231694

Authors

  • Hu Y
  • Ota N
  • Peng I
  • Refino CJ
  • Danilenko DM
  • Caplazi P
  • Ouyang W

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Data

April 15, 2010

Associated Grants

None

Mesh Terms

  • Animals
  • Cell Line, Transformed
  • Cells, Cultured
  • Central Nervous System
  • Coculture Techniques
  • Encephalomyelitis, Autoimmune, Experimental
  • Humans
  • Interleukin-17
  • Interleukins
  • Mice
  • Mice, Congenic
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Molecular Sequence Data
  • Receptors, Interleukin
  • Signal Transduction