TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease - Wikidata - wikimedia - TriplyDB

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

http://www.wikidata.org/entity/Q36639973

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Therapeutic Treg expansion in mice by TNFRSF25 prevents allergic lung inflammation Cytokine and anti-cytokine therapies in prevention or treatment of fibrosis in IBD The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator Membrane trafficking of death receptors: implications on signalling Biochemical and Structural Characterization of the Human TL1A Ectodomain ,Decoy Strategies: The Structure of TL1A:DcR3 Complex On death receptor 3 and its ligands…TNFRSF25 agonistic antibody and galectin-9 combination therapy controls herpes simplex virus-induced immunoinflammatory lesions R-flurbiprofen attenuates experimental autoimmune encephalomyelitis in mice The role of tumor necrosis factor receptor superfamily members in mammalian brain development, function and homeostasis Predicting HLA alleles from high-resolution SNP data in three Southeast Asian populations.IBD-associated TL1A gene (TNFSF15) haplotypes determine increased expression of TL1A protein.TLR8-mediated activation of human monocytes inhibits TL1A expression.Constitutive TL1A (TNFSF15) expression on lymphoid or myeloid cells leads to mild intestinal inflammation and fibrosis Tumour necrosis factor superfamily members in the pathogenesis of inflammatory bowel disease The TNF-like protein 1A-death receptor 3 pathway promotes macrophage foam cell formation in vitro.Age-dependent maintenance of motor control and corticostriatal innervation by death receptor 3.Insights into IBD Pathogenesis.CX₃CR1⁺ mononuclear phagocytes support colitis-associated innate lymphoid cell production of IL-22.Two functionally distinct isoforms of TL1A (TNFSF15) generated by differential ectodomain shedding T cell stimulator cells, an efficient and versatile cellular system to assess the role of costimulatory ligands in the activation of human T cells.Naive and activated T cells display differential responsiveness to TL1A that affects Th17 generation, maintenance, and proliferation.TL1-A can engage death receptor-3 and activate NF-kappa B in endothelial cells.The TNF-family cytokine TL1A inhibits proliferation of human activated B cells The adaptor protein TRADD is essential for TNF-like ligand 1A/death receptor 3 signaling.c-Myc is essential to prevent endothelial pro-inflammatory senescent phenotype.Progranulin-derived Atsttrin directly binds to TNFRSF25 (DR3) and inhibits TNF-like ligand 1A (TL1A) activity.Central role of IL-17/Th17 immune responses and the gut microbiota in the pathogenesis of intestinal fibrosis Natural positive selection and north-south genetic diversity in East Asia.TNF superfamily in inflammatory disease: translating basic insights.Constitutive TL1A expression under colitogenic conditions modulates the severity and location of gut mucosal inflammation and induces fibrostenosis.Megakaryocyte progenitors are the main APCs inducing Th17 response to lupus autoantigens and foreign antigens Fine-mapping analysis revealed complex pleiotropic effect and tissue-specific regulatory mechanism of TNFSF15 in primary biliary cholangitis, Crohn's disease and leprosy.Human group3 innate lymphoid cells express DR3 and respond to TL1A with enhanced IL-22 production and IL-2-dependent proliferation.The TNF-family cytokine TL1A drives IL-13-dependent small intestinal inflammation.TNFSF15 Modulates Neovascularization and Inflammation Directed evolution of a soluble human DR3 receptor for the inhibition of TL1A induced cytokine secretion Differential Levels of Tl1a Affect the Expansion and Function of Regulatory T Cells in Modulating Murine Colitis SUSTAINED TL1A (TNFSF15) EXPRESSION ON BOTH LYMPHOID AND MYELOID CELLS LEADS TO MILD SPONTANEOUS INTESTINAL INFLAMMATION AND FIBROSIS.Transmembrane TNF-TNFR2 Impairs Th17 Differentiation by Promoting Il2 Expression.

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TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

http://www.wikidata.org/entity/Q36639973

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

@zh-cn

name

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

@ast

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

@en

type

label

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

@ast

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

@en

prefLabel

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

@ast

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

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Journal of Experimental Medicine

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TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

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P2093

Anna Borodovsky

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

Beth Browning

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

Bhanu P Pappu

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

Chen Dong

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

Li Ma

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

Lihe Su

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

Linda C Burkly

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Martin L Scott

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Pascal Schneider

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Ping Wu

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

P2860

VEGI, a novel cytokine of the tumor necrosis factor family, is an angiogenesis inhibitor that suppresses the growth of colon carcinomas in vivo

TL1A is a TNF-like ligand for DR3 and TR6/DcR3 and functions as a T cell costimulator

Signal transduction by DR3, a death domain-containing receptor related to TNFR-1 and CD95

LARD: a new lymphoid-specific death domain containing receptor regulated by alternative pre-mRNA splicing

TRAMP, a novel apoptosis-mediating receptor with sequence homology to tumor necrosis factor receptor 1 and Fas(Apo-1/CD95)

Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells

Expression of silencer of death domains and death-receptor-3 in normal human kidney and in rejecting renal transplants

Cell fate decision: T-helper 1 and 2 subsets in immune responses.

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

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1049-1062

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10.1084/JEM.20071364

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P433

5

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205

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2008-04-14T00:00:00Z

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5442039

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18411337

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2373838

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