The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis. - Wikidata - wikimedia - TriplyDB

The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

http://www.wikidata.org/entity/Q35441559

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Recent advances in understanding the molecular mechanisms of the development and function of Th17 cells CCR2 deficiency promotes exacerbated chronic erosive neutrophil-dominated chikungunya virus arthritis Regulation of the Adaptive Immune Response by the IκB Family Protein Bcl-3 Regulation of IL-17 in autoimmune diseases by transcriptional factors and microRNAs Regulation of nuclear factor-κB in autoimmunity Diversity of IL-17-producing T lymphocytes NF-κB in inflammation and renal diseases Genetic requirements for the development and differentiation of interleukin-17-producing γδ T cells A key role for NF-κB transcription factor c-Rel in T-lymphocyte-differentiation and effector functions NF-κB Pathways in the Pathogenesis of Multiple Sclerosis and the Therapeutic Implications TCR signaling to NF-κB and mTORC1: Expanding roles of the CARMA1 complex Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis.A small-molecule c-Rel inhibitor reduces alloactivation of T cells without compromising antitumor activity Toll-like receptor 6 stimulation promotes T-helper 1 and 17 responses in gastrointestinal-associated lymphoid tissue and modulates murine experimental colitis BET bromodomain inhibition suppresses TH17-mediated pathology.Cleavage of roquin and regnase-1 by the paracaspase MALT1 releases their cooperatively repressed targets to promote T(H)17 differentiation.The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of autoimmune T cells Control of Toll-like receptor-mediated T cell-independent type 1 antibody responses by the inducible nuclear protein IκB-ζ Aryl hydrocarbon receptor promotes RORγt⁺ group 3 ILCs and controls intestinal immunity and inflammation.Calcium signaling via Orai1 is essential for induction of the nuclear orphan receptor pathway to drive Th17 differentiation Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A.The nuclear IκB family protein IκBNS influences the susceptibility to experimental autoimmune encephalomyelitis in a murine model Inhibition of RORγt activity and Th17 differentiation by a set of novel compounds.Distribution of T Cells in Rainbow Trout (Oncorhynchus mykiss) Skin and Responsiveness to Viral Infection.Negative Immune Regulator TIPE2 Promotes M2 Macrophage Differentiation through the Activation of PI3K-AKT Signaling Pathway Hypoxia-inducible factor-1 alpha-dependent induction of FoxP3 drives regulatory T-cell abundance and function during inflammatory hypoxia of the mucosa IMMUNODEFICIENCIES. Impairment of immunity to Candida and Mycobacterium in humans with bi-allelic RORC mutations.Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.T cell receptor/CARMA1/NF-κB signaling controls T-helper (Th) 17 differentiation PDLIM2 restricts Th1 and Th17 differentiation and prevents autoimmune disease.Nuclear matrix protein SMAR1 control regulatory T-cell fate during inflammatory bowel disease (IBD)HVEM: An unusual TNF receptor family member important for mucosal innate immune responses to microbes.Transcriptome signature for dampened Th2 dominance in acellular pertussis vaccine-induced CD4(+) T cell responses through TLR4 ligation.Lipopolysaccharide-Induced Chorioamnionitis Promotes IL-1-Dependent Inflammatory FOXP3+ CD4+ T Cells in the Fetal Rhesus Macaque.The aryl hydrocarbon receptor: a novel target for immunomodulation in organ transplantation.Toll/Interleukin-1 Receptor Domain Derived from TcpC (TIR-TcpC) Ameliorates Experimental Autoimmune Arthritis by Down-modulating Th17 Cell Response.Xianfanghuomingyin, a Chinese Compound Medicine, Modulates the Proliferation and Differentiation of T Lymphocyte in a Collagen-Induced Arthritis Mouse Model.c-Rel in GVHD biology: a missing link.Impact of the gut microbiota on enhancer accessibility in gut intraepithelial lymphocytes.c-Rel is an essential transcription factor for the development of acute graft-versus-host disease in mice.

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The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

http://www.wikidata.org/entity/Q35441559

description

2011 nî lūn-bûn

@nan

2011 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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type

label

The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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prefLabel

The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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The Th17 immune response is controlled by the Rel-RORγ-RORγ T transcriptional axis.

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Amer A Beg

http://www.w3.org/2001/XMLSchema#string

Hsiou-Chi Liou

http://www.w3.org/2001/XMLSchema#string

Jennifer DeVirgiliis

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Jing Sun

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Junmei Wang

http://www.w3.org/2001/XMLSchema#string

Qingguo Ruan

http://www.w3.org/2001/XMLSchema#string

Shijun Zheng

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Vasumathi Kameswaran

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Yan Zhang

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Youhai H Chen

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P2860

RORgamma t, a novel isoform of an orphan receptor, negatively regulates Fas ligand expression and IL-2 production in T cells

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells

RORgammaT, a thymus-specific isoform of the orphan nuclear receptor RORgamma / TOR, is up-regulated by signaling through the pre-T cell receptor and binds to the TEA promoter

STAT3 and NF-kappaB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice

Genomic structure and chromosomal mapping of the nuclear orphan receptor ROR gamma (RORC) gene

STAT3 regulates cytokine-mediated generation of inflammatory helper T cells

TAK1, but not TAB1 or TAB2, plays an essential role in multiple signaling pathways in vivo.

T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma

TIPE2, a negative regulator of innate and adaptive immunity that maintains immune homeostasis

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10.1084/JEM.20110462

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22006976

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