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Title[redir]:
Fate mapping of IL-17-producing T cells in inflammatory responses | Nature Immunology
Description:
Although in vitro–generated cells of the TH17 helper T cell subset are highly plastic, it is unclear whether TH17 cells that develop in vivo retain their phenotype. To investigate this, Stockinger and colleagues have generated a TH17 reporter system to map the fate of these cells in vivo. 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 (TH17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in TH17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of TH17 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 (
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article, google, scholar, cells, cas, nature, cell, immunol, autoimmune, med, research, helper, nat, exp, immunity, interleukin, encephalomyelitis, access, lineage, differentiation, ilproducing, experimental, inflammation, content, veldhoen, plasticity, medical, cookies, fate, inflammatory, stockinger, development, effector, privacy, immunology, receptor, institute, council, supplementary, data, information, january, mapping, hirota, alexandre, potocnik, brigitta, mouse, distinct, eae,
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nature portfolio permissions reprints privacy policy biological services regional cns responses provided il-23p19-deficient mice advertising th17 cell-derived tgf-β1 interferon-γ-producing th1 subset social media nature 452 nature 467 nature european research council il-17f-creeyfp reporter mouse nod/scid recipient mice short-lived th17 cells myelin oligodendrocyte glycoprotein-specific codon-improved cre recombinase medical research data protection experimental autoimmune encephalomyelitis personal data helper cell subsets central nervous system pd-1 positive microglia cancer research mediate autoimmune encephalomyelitis springerlink instant access permissions experimental autoimmune encephalitis human th17 cells autoimmune th17 cells th1 cell functions ifn-γ chronic inflammatory conditions induce diabetes efficiently th17 cell differentiation 5nod mice convert human il-17-producing dendritic cells inhibits cell lineage differentiation privacy 17 cell-mediated pathology aryl hydrocarbon receptor acute cutaneous infection present address competing financial interests th17 developmental origin explore content
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headline:Fate mapping of IL-17-producing T cells in inflammatory responses
description:Although in vitroâgenerated cells of the TH17 helper T cell subset are highly plastic, it is unclear whether TH17 cells that develop in vivo retain their phenotype. To investigate this, Stockinger and colleagues have generated a TH17 reporter system to map the fate of these cells in vivo. 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 (TH17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in TH17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of TH17 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-TH17 cells'). Thus, this model allows the actual functional fate of effector T cells to be related to TH17 developmental origin regardless of IL-17 expression.
datePublished:2011-01-30T00:00:00Z
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Interleukins
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description:Although in vitroâgenerated cells of the TH17 helper T cell subset are highly plastic, it is unclear whether TH17 cells that develop in vivo retain their phenotype. To investigate this, Stockinger and colleagues have generated a TH17 reporter system to map the fate of these cells in vivo. 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 (TH17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in TH17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of TH17 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-TH17 cells'). Thus, this model allows the actual functional fate of effector T cells to be related to TH17 developmental origin regardless of IL-17 expression.
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Interleukins
T-helper 17 cells
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Infectious Diseases
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