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Nat Immunol. 2011 Mar;12(3):255-63. doi: 10.1038/ni.1993. Epub 2011 Jan 30.

Fate mapping of IL-17-producing T cells in inflammatory responses.

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1
Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, Mill Hill, London, UK.

Abstract

Here we describe a reporter mouse strain designed to map the fate of cells that have activated interleukin 17A (IL-17A). We found that IL-17-producing helper T cells (T(H)17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in T(H)17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of T(H)17 cells to the production of alternative cytokines, although IL-17A production was shut off in the course of the infection. During the development of EAE, interferon-γ (IFN-γ) and other proinflammatory cytokines in the spinal cord were produced almost exclusively by cells that had produced IL-17 before their conversion by IL-23 ('ex-T(H)17 cells'). Thus, this model allows the actual functional fate of effector T cells to be related to T(H)17 developmental origin regardless of IL-17 expression.

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PMID:
21278737
PMCID:
PMC3040235
DOI:
10.1038/ni.1993
[Indexed for MEDLINE]
Free PMC Article

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