Journal
NATURE IMMUNOLOGY
Volume 6, Issue 11, Pages 1133-1141Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1261
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Funding
- NIAID NIH HHS [R01 AI050746, R01 AI050761] Funding Source: Medline
- NIAMS NIH HHS [R01 AR050772] Funding Source: Medline
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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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