Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis. - Wikidata - wikimedia - TriplyDB

Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis.

Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis.

http://www.wikidata.org/entity/Q36403957

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Foxp3 interacts with nuclear factor of activated T cells and NF-kappa B to repress cytokine gene expression and effector functions of T helper cells The transcription factors T-bet and GATA-3 control alternative pathways of T-cell differentiation through a shared set of target genes Generation of pathogenic T(H)17 cells in the absence of TGF-β signalling Tumor-specific Th17-polarized cells eradicate large established melanoma Dysregulated T cell expression of TIM3 in multiple sclerosis APC-derived cytokines and T cell polarization in autoimmune inflammation The Mucosal Immune System and Its Regulation by Autophagy Advances in T Helper 17 Cell Biology: Pathogenic Role and Potential Therapy in Multiple Sclerosis γδ T Cells and NK Cells - Distinct Pathogenic Roles as Innate-Like Immune Cells in CNS Autoimmunity Stage-Specific Role of Interferon-Gamma in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis The regulation of inflammation by interferons and their STATs Pouring fuel on the fire: Th17 cells, the environment, and autoimmunity Jakpot! New small molecules in autoimmune and inflammatory diseases Design of oral agents for the management of multiple sclerosis: benefit and risk assessment for dimethyl fumarate T-bet represses T(H)17 differentiation by preventing Runx1-mediated activation of the gene encoding RORγt Marking and quantifying IL-17A-producing cells in vivo RTL551 treatment of EAE reduces CD226 and T-bet+ CD4 T cells in periphery and prevents infiltration of T-bet+ IL-17, IFN-γ producing T cells into CNS Tumor necrosis factor-α produced in the kidney contributes to angiotensin II-dependent hypertension.IFN-gamma and STAT1 arrest monocyte migration and modulate RAC/CDC42 pathways IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-beta.The role of the Th1 transcription factor T-bet in a mouse model of immune-mediated bone-marrow failure T-bet and eomesodermin play critical roles in directing T cell differentiation to Th1 versus Th17.More stories on Th17 cells.IFN-gamma regulates the requirement for IL-17 in proteoglycan-induced arthritis.Role of the innate immune system in the pathogenesis of multiple sclerosis.Mechanisms of intestinal inflammation and development of associated cancers: lessons learned from mouse models.Involvement of the janus kinase/signal transducer and activator of transcription signaling pathway in multiple sclerosis and the animal model of experimental autoimmune encephalomyelitis.Interferon-γ inhibits central nervous system myelination through both STAT1-dependent and STAT1-independent pathways BCL6 controls Th9 cell development by repressing Il9 transcription.Treatment with the antipsychotic agent, risperidone, reduces disease severity in experimental autoimmune encephalomyelitis.Th1 and Th17 cells: adversaries and collaborators Inflammation programs self-reactive CD8+ T cells to acquire T-box-mediated effector function but does not prevent deletional tolerance Current views on the roles of Th1 and Th17 cells in experimental autoimmune encephalomyelitis.EAE mediated by a non-IFN-γ/non-IL-17 pathway.Interferon-β exacerbates Th17-mediated inflammatory disease.Transcriptional modulation of the immune response by peroxisome proliferator-activated receptor-{alpha} agonists in autoimmune disease.Characterization of autoreactive and bystander IL-17+ T cells induced in immunized C57BL/6 mice.Transcription factor T-bet regulates inflammatory arthritis through its function in dendritic cells.Exogenous IFN-gamma ex vivo shapes the alloreactive T-cell repertoire by inhibition of Th17 responses and generation of functional Foxp3+ regulatory T cells Decreased signal transducers and activators of transcription (STAT) protein expression in lymphatic organs during EAE development in mice.

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P2860

Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis.

http://www.wikidata.org/entity/Q36403957

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年學術文章

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2004年學術文章

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2004年學術文章

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name

Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

@ast

Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

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type

label

Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

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Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

@en

prefLabel

Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

@ast

Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

@en

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Loss of T-bet, but not STAT1, ...... autoimmune encephalomyelitis.

@en

P2093

Brandon Sullivan

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

Estelle Bettelli

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

Laurie H Glimcher

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

Raymond A Sobel

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Susanne J Szabo

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Vijay K Kuchroo

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P2860

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

Impaired development of CD4+ CD25+ regulatory T cells in the absence of STAT1: increased susceptibility to autoimmune disease.

Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway

Signaling and transcription in T helper development.

T-bet is rapidly induced by interferon-gamma in lymphoid and myeloid cells

The molecular basis of T helper 1 and T helper 2 cell differentiation.

IFNs and STATs in innate immunity to microorganisms.

Acquisition of lymphokine-producing phenotype by CD4+ T cells.

T-bet is required for optimal production of IFN-gamma and antigen-specific T cell activation by dendritic cells

Control of autoimmunity by naturally arising regulatory CD4+ T cells.

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15238607

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experimental autoimmune encephalomyelitis

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2213316

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