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

Authors: Park, H  Li, Z  Yang, XO  Chang, SH  Nurieva, R  Wang, YH  Wang, Y  Hood, L  Zhu, Z  Tian, Q  Dong, C 
Citation: Park H, etal., Nat Immunol. 2005 Nov;6(11):1133-41. Epub 2005 Oct 2.
Pubmed: (View Article at PubMed) PMID:16200068
DOI: Full-text: DOI:10.1038/ni1261

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-gamma 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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CRRD Object Information
CRRD ID: 9212317
Created: 2014-08-25
Species: All species
Last Modified: 2014-08-25
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.