Treatment with IL-17 prolongs the half-life of chemokine CXCL1 mRNA via the adaptor TRAF5 and the splicing-regulatory factor SF2 (ASF)

Nat Immunol. 2011 Aug 7;12(9):853-60. doi: 10.1038/ni.2081.

Abstract

Interleukin 17 (IL-17) promotes the expression of chemokines and cytokines via the induction of gene transcription and post-transcriptional stabilization of mRNA. We show here that IL-17 enhanced the stability of chemokine CXCL1 mRNA and other mRNAs through a pathway that involved the adaptor Act1, the adaptors TRAF2 or TRAF5 and the splicing factor SF2 (also known as alternative splicing factor (ASF)). TRAF2 and TRAF5 were necessary for IL-17 to signal the stabilization of CXCL1 mRNA. Furthermore, IL-17 promoted the formation of complexes of TRAF5-TRAF2, Act1 and SF2 (ASF). Overexpression of SF2 (ASF) shortened the half-life of CXCL1 mRNA, whereas depletion of SF2 (ASF) prolonged it. SF2 (ASF) bound chemokine mRNA in unstimulated cells, whereas the SF2 (ASF)-mRNA interaction was much lower after stimulation with IL-17. Our findings define an IL-17-induced signaling pathway that links to the stabilization of selected mRNA species through Act1, TRAF2-TRAF5 and the RNA-binding protein SF2 (ASF).

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / immunology
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Alternative Splicing
  • Animals
  • Chemokine CXCL1 / genetics
  • Chemokine CXCL1 / immunology
  • Chemokine CXCL1 / metabolism*
  • Female
  • Half-Life
  • HeLa Cells
  • Humans
  • Inflammation / genetics
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Interleukin-17* / immunology
  • Interleukin-17* / metabolism
  • Interleukin-17* / pharmacology
  • Mice
  • Mice, Knockout
  • Nuclear Proteins / genetics
  • Nuclear Proteins / immunology
  • Nuclear Proteins / metabolism*
  • RNA Processing, Post-Transcriptional
  • RNA Stability / drug effects
  • RNA, Messenger
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / immunology
  • RNA-Binding Proteins / metabolism*
  • Serine-Arginine Splicing Factors
  • Signal Transduction / immunology*
  • TNF Receptor-Associated Factor 5 / genetics
  • TNF Receptor-Associated Factor 5 / immunology
  • TNF Receptor-Associated Factor 5 / metabolism*
  • Th17 Cells / immunology*
  • Th17 Cells / metabolism
  • Transcription, Genetic

Substances

  • Adaptor Proteins, Signal Transducing
  • Chemokine CXCL1
  • Interleukin-17
  • Nuclear Proteins
  • RNA, Messenger
  • RNA-Binding Proteins
  • T2bp protein, mouse
  • TNF Receptor-Associated Factor 5
  • Traf3ip2 protein, mouse
  • Serine-Arginine Splicing Factors