Affordable Access

Access to the full text

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

Authors
  • Park, Heon1
  • Li, Zhaoxia1
  • Yang, Xuexian O2
  • Chang, Seon Hee2
  • Nurieva, Roza2
  • Wang, Yi-Hong2
  • Wang, Ying1
  • Hood, Leroy3
  • Zhu, Zhou4
  • Tian, Qiang3
  • Dong, Chen2
  • 1 University of Washington, Seattle, Washington, 98195, USA , Seattle (United States)
  • 2 MD Anderson Cancer Center, Houston, Texas, 77030, USA , Houston (United States)
  • 3 Institute for Systems Biology, Seattle, Washington, 98103, USA , Seattle (United States)
  • 4 Johns Hopkins University School of Medicine, Baltimore, Maryland, 21224, USA , Baltimore (United States)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Oct 02, 2005
Volume
6
Issue
11
Pages
1133–1141
Identifiers
DOI: 10.1038/ni1261
Source
Springer Nature
License
Yellow

Abstract

Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-γ negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.

Report this publication

Statistics

Seen <100 times