Nature Immunology 6, 1133 - 1141 (2005)
Published online: 2 October 2005; | doi:10.1038/ni1261
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17Heon Park1, 5, Zhaoxia Li1, 5, Xuexian O Yang2, 5, Seon Hee Chang2, Roza Nurieva2, Yi-Hong Wang2, Ying Wang1, Leroy Hood3, Zhou Zhu4, Qiang Tian3
& Chen Dong21
Department of Immunology, University of Washington, Seattle, Washington 98195, USA. 2
Department of Immunology, MD Anderson Cancer Center, Houston, Texas 77030, USA. 3
Institute for Systems Biology, Seattle, Washington 98103, USA. 4
Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA. 5
These authors contributed equally to this work.
Correspondence should be addressed to Chen Dong cdong@mdanderson.org 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- 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.
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