STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation. - Wikidata - awgldk - TriplyDB

STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation.

STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation.

http://www.wikidata.org/entity/Q34660034

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Integrating Immunologic Signaling Networks: The JAK/STAT Pathway in Colitis and Colitis-Associated Cancer Th17 Cells Pathways in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders: Pathophysiological and Therapeutic Implications Novel Insights and Therapeutics in Multiple Sclerosis Maintenance of Immune Homeostasis through ILC/T Cell Interactions Pivotal roles of GM-CSF in autoimmunity and inflammation GM-CSF: An immune modulatory cytokine that can suppress autoimmunity Circulating immune cells in multiple sclerosis.Functional inflammatory profiles distinguish myelin-reactive T cells from patients with multiple sclerosis STAT4 controls GM-CSF production by both Th1 and Th17 cells during EAE.Autoreactive T Cells from Patients with Myasthenia Gravis Are Characterized by Elevated IL-17, IFN-γ, and GM-CSF and Diminished IL-10 Production.IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis Aging diminishes the resistance of AO rats to EAE: putative role of enhanced generation of GM-CSF Expressing CD4+ T cells in aged rats.GM-CSF-Producing Th Cells in Rats Sensitive and Resistant to Experimental Autoimmune Encephalomyelitis.Age-Related Differences in Percentages of Regulatory and Effector T Lymphocytes and Their Subsets in Healthy Individuals and Characteristic STAT1/STAT5 Signalling Response in Helper T Lymphocytes IL-22, GM-CSF and IL-17 in peripheral CD4+ T cell subpopulations during multiple sclerosis relapses and remission. Impact of corticosteroid therapy.Impact of Notch1 Deletion in Macrophages on Proinflammatory Cytokine Production and the Outcome of Experimental Autoimmune Encephalomyelitis.Alterations of the human gut microbiome in multiple sclerosis.TGF-β Affects the Differentiation of Human GM-CSF+ CD4+ T Cells in an Activation- and Sodium-Dependent Manner Opportunities for Translation from the Bench: Therapeutic Intervention of the JAK/STAT Pathway in Neuroinflammatory Diseases.Immortalization of primary microglia: a new platform to study HIV regulation in the central nervous system.GM-CSF as a target in inflammatory/autoimmune disease: current evidence and future therapeutic potential.Harnessing the Therapeutic Potential of Th17 Cells.Targeting GM-CSF in inflammatory diseases.Mechanism of TH2/TH17-predominant and neutrophilic TH2/TH17-low subtypes of asthma.STAT5 and CD4 + T Cell Immunity.AMP-Activated Protein Kinase Suppresses Autoimmune Central Nervous System Disease by Regulating M1-Type Macrophage-Th17 Axis.CCR6+ Th cells in the cerebrospinal fluid of persons with multiple sclerosis are dominated by pathogenic non-classic Th1 cells and GM-CSF-only-secreting Th cells.Tetrandrine, an agonist of aryl hydrocarbon receptor, reciprocally modulates the activities of STAT3 and STAT5 to suppress Th17 cell differentiation.Producing GM-CSF: a unique T helper subset?A T Cell View of the Bone Marrow.Response to Treatment with TNFα Inhibitors in Rheumatoid Arthritis Is Associated with High Levels of GM-CSF and GM-CSF+ T Lymphocytes.Foxo3 Transcription Factor Drives Pathogenic T Helper 1 Differentiation by Inducing the Expression of Eomes.PD-1 Controls Tonic Signaling and Lymphopenia-Induced Proliferation of T Lymphocytes.OMIP-030: Characterization of human T cell subsets via surface markers.Cytokine Signaling in Multiple Sclerosis and Its Therapeutic Applications.Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis.GM-CSF as a therapeutic target in autoimmune diseases.BATF-dependent IL-7RhiGM-CSF+ T cells control intestinal graft-versus-host disease.Mesenteric injection of adipose-derived mesenchymal stem cells relieves experimentally-induced colitis in rats by regulating Th17/Treg cell balance.Targeting Inflammatory T Helper Cells via Retinoic Acid-Related Orphan Receptor Gamma t Is Ineffective to Prevent Allo-Response-Driven Colitis.

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STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation.

http://www.wikidata.org/entity/Q34660034

description

2014 nî lūn-bûn

@nan

2014 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

@wuu

name

STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

@en

STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

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type

label

STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

@en

STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

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prefLabel

STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

@en

STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

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STAT5 programs a distinct subs ...... autoimmune neuroinflammation.

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P2093

Akira Moh

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

David Michael Kemeny

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

Fan Yang

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

Henry Yang

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

Mark H Kaplan

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Patrick Tan

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Pey Yng Low

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Wanqiang Sheng

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Xin-Yuan Fu

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Yi Zhou

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

P2860

A novel transcription factor, T-bet, directs Th1 lineage commitment

Transgenic mice for interleukin 3 develop motor neuron degeneration associated with autoimmune reaction against spinal cord motor neurons

The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo

Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5

Th17 and regulatory T cells in mediating and restraining inflammation.

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

TH17 cells in development: an updated view of their molecular identity and genetic programming

STAT3 regulates cytokine-mediated generation of inflammatory helper T cells

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

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1387-1402

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10.1038/CR.2014.154

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25412660

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