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Open AccessJournal ArticleDOI

TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-Producing T cells

TLDR
The data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation ofIL-17-producing T cells.
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This article is published in Immunity.The article was published on 2006-02-01 and is currently open access. It has received 3711 citations till now. The article focuses on the topics: IL-2 receptor & Cytotoxic T cell.

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Exploring the full spectrum of macrophage activation.

TL;DR: This Review suggests a new grouping of macrophages based on three different homeostatic activities — host defence, wound healing and immune regulation, and proposes that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation.
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Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.

TL;DR: It is shown that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ Treg cells induced by TGF-β, and the data demonstrate a dichotomy in thegeneration of pathogenic (TH17) T cells that induce autoimmunity and regulatory (Foxp3+) T Cells that inhibit autoimmune tissue injury.
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The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.

TL;DR: It is shown that the orphan nuclear receptor RORgammat is the key transcription factor that orchestrates the differentiation of this effector cell lineage of proinflammatory T helper cells and its potential as a therapeutic target in inflammatory diseases is highlighted.
Journal ArticleDOI

IL-17 and Th17 Cells.

TL;DR: The investigation of the differentiation, effector function, and regulation of Th17 cells has opened up a new framework for understanding T cell differentiation and now appreciate the importance of Th 17 cells in clearing pathogens during host defense reactions and in inducing tissue inflammation in autoimmune disease.
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Regulatory T Cells and Immune Tolerance

TL;DR: The cellular and molecular basis of Treg development and function is revealed and dysregulation of T Regs in immunological disease is implicates.
References
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Journal ArticleDOI

Interleukin-10 and the interleukin-10 receptor.

TL;DR: Findings that have advanced the understanding of IL-10 and its receptor are highlighted, as well as its in vivo function in health and disease.
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Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

TL;DR: Current understanding on the mechanisms of TGF-β signaling from cell membrane to the nucleus is presented and the transcriptional regulation of target gene expression is reviewed.
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Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

TL;DR: 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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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

TL;DR: 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, indicating a unique T helper lineage that regulates tissue inflammation.
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

TL;DR: Using passive transfer studies, it is confirmed that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.
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