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

Heon Park, Zhaoxia Li, Xuexian O. Yang, Seon Hee Chang, Roza Nurieva, Yi Hong Wang, Ying Wang, Leroy Hood, Zhou Zhu, Qiang Tian, Chen Dong

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)1133-1141
Number of pages9
JournalNature Immunology
Volume6
Issue number11
DOIs
StatePublished - Nov 2005

Fingerprint

Interleukin-17
Inflammation
T-Lymphocytes
Helper-Inducer T-Lymphocytes
Chemokines
Autoimmune Experimental Encephalomyelitis
Interleukin-4
Interferons
Autoimmune Diseases
Leukocytes
Transcription Factors
Epithelium
Cytokines
Lung
Antibodies
Brain

ASJC Scopus subject areas

  • Immunology

Cite this

Park, H., Li, Z., Yang, X. O., Chang, S. H., Nurieva, R., Wang, Y. H., ... Dong, C. (2005). A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nature Immunology, 6(11), 1133-1141. https://doi.org/10.1038/ni1261

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. / Park, Heon; Li, Zhaoxia; Yang, Xuexian O.; Chang, Seon Hee; Nurieva, Roza; Wang, Yi Hong; Wang, Ying; Hood, Leroy; Zhu, Zhou; Tian, Qiang; Dong, Chen.

In: Nature Immunology, Vol. 6, No. 11, 11.2005, p. 1133-1141.

Research output: Contribution to journalArticle

Park, H, Li, Z, Yang, XO, Chang, SH, Nurieva, R, Wang, YH, Wang, Y, Hood, L, Zhu, Z, Tian, Q & Dong, C 2005, 'A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17', Nature Immunology, vol. 6, no. 11, pp. 1133-1141. https://doi.org/10.1038/ni1261
Park, Heon ; Li, Zhaoxia ; Yang, Xuexian O. ; Chang, Seon Hee ; Nurieva, Roza ; Wang, Yi Hong ; Wang, Ying ; Hood, Leroy ; Zhu, Zhou ; Tian, Qiang ; Dong, Chen. / A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. In: Nature Immunology. 2005 ; Vol. 6, No. 11. pp. 1133-1141.
@article{af52c94542dd44bbba59744784e45455,
title = "A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17",
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.",
author = "Heon Park and Zhaoxia Li and Yang, {Xuexian O.} and Chang, {Seon Hee} and Roza Nurieva and Wang, {Yi Hong} and Ying Wang and Leroy Hood and Zhou Zhu and Qiang Tian and Chen Dong",
year = "2005",
month = "11",
doi = "10.1038/ni1261",
language = "English (US)",
volume = "6",
pages = "1133--1141",
journal = "Nature Immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "11",

}

TY - JOUR

T1 - A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

AU - Park, Heon

AU - Li, Zhaoxia

AU - Yang, Xuexian O.

AU - Chang, Seon Hee

AU - Nurieva, Roza

AU - Wang, Yi Hong

AU - Wang, Ying

AU - Hood, Leroy

AU - Zhu, Zhou

AU - Tian, Qiang

AU - Dong, Chen

PY - 2005/11

Y1 - 2005/11

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=27544465354&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=27544465354&partnerID=8YFLogxK

U2 - 10.1038/ni1261

DO - 10.1038/ni1261

M3 - Article

VL - 6

SP - 1133

EP - 1141

JO - Nature Immunology

JF - Nature Immunology

SN - 1529-2908

IS - 11

ER -