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Title:
Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages | Nature Immunology
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CD4+ T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (TH1) or TH2 lineages and instead favor the idea of a distinct effector lineage we call
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nature portfolio permissions reprints privacy policy th17 cell-derived tgf-β1 advertising social media nature 421 nature author information authors jak-stat signaling pathway tlr-activated dendritic cells author correspondence proximal ifn-gamma promoter t-helper 1 development–resolved silencing t-bet defines disrupted interferon-γ genes disrupted ifn-γ gene delayed-type hypersensitivity responses cd4+cd8+tcrlo thymocytes data protection promote ifn-γ production springerlink instant access permissions il-12p35-deficient mice counting antigen-specific cd8 personal data rocaglamide promotes infiltration il-4-independent mechanism joint autoimmune inflammation th1 development mediated present data experimental autoimmune encephalomyelitis induces autoimmune inflammation enhanced th1 development th17 cell heterogeneity biological activities similar privacy transcription factor gata-3 il-26+ th17 intermediates competing financial interests il-17-producing cells shared developmental pathway issue learn il-12-dependent selection ifn-γ plays ifn-α signal ifn-γ production interleukin-23 promotes independent mechanisms european economic area
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headline:Interleukin 17âproducing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
description:CD4+ T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (TH1) or TH2 lineages and instead favor the idea of a distinct effector lineage we call 'TH-17'. The development of TH-17 cells from naive precursor cells was potently inhibited by interferon-γ (IFN-γ) and IL-4, whereas committed TH-17 cells were resistant to suppression by TH1 or TH2 cytokines. In the absence of IFN-γ and IL-4, IL-23 induced naive precursor cells to differentiate into TH-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
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description:CD4+ T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (TH1) or TH2 lineages and instead favor the idea of a distinct effector lineage we call 'TH-17'. The development of TH-17 cells from naive precursor cells was potently inhibited by interferon-γ (IFN-γ) and IL-4, whereas committed TH-17 cells were resistant to suppression by TH1 or TH2 cytokines. In the absence of IFN-γ and IL-4, IL-23 induced naive precursor cells to differentiate into TH-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
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