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The Cytokine IL-17A Limits Th17 Pathogenicity via a Negative Feedback Loop Driven by Autocrine Induction of IL-24

Authors
  • Chong, Wai Po1, 2
  • Mattapallil, Mary J.2
  • Raychaudhuri, Kumarkrishna2
  • Bing, So Jin2
  • Wu, Sihan1
  • Zhong, Yajie1
  • Wang, WeiWei1
  • Chen, Zilin1
  • Silver, Phyllis B.2
  • Jittayasothorn, Yingyos2
  • Chan, Chi-Chao2
  • Chen, Jun1
  • Horai, Reiko2
  • Caspi, Rachel R.2
  • 1 State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, China
  • 2 Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-1857, USA
Type
Published Article
Journal
Immunity
Publication Date
Jul 15, 2020
Volume
53
Issue
2
Pages
384–397
Identifiers
DOI: 10.1016/j.immuni.2020.06.022
PMID: 32673565
PMCID: PMC7362799
Source
PubMed Central
Keywords
Disciplines
  • Article
License
Unknown

Abstract

Loss of IL-17A, the signature cytokine of autoreactive Th17 cells, unexpectedly did not diminish the pathogenicity of Th17 cells in neuroinflammatory disease. This report demonstrates that IL-17A represses the Th17 cytokine program, primarily IL-17F and GM-CSF, by inducing autocrine production of IL-24. Thus, IL-17A has a dual role in Th17 cells: pathogenic as well as regulatory.

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