EAE mediated by a non-IFN-γ/non-IL-17 pathway. - Wikidata - awgldk - TriplyDB

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

http://www.wikidata.org/entity/Q34142931

about

CXCR7 influences leukocyte entry into the CNS parenchyma by controlling abluminal CXCL12 abundance during autoimmunity Innate immunity in the central nervous system The NLRP12 Sensor Negatively Regulates Autoinflammatory Disease by Modulating Interleukin-4 Production in T Cells.Myeloid cell transmigration across the CNS vasculature triggers IL-1β-driven neuroinflammation during autoimmune encephalomyelitis in mice.Batf3-dependent CD11b(low/-) peripheral dendritic cells are GM-CSF-independent and are not required for Th cell priming after subcutaneous immunization.Bhlhe40 controls cytokine production by T cells and is essential for pathogenicity in autoimmune neuroinflammation.Chemokine receptor expression by inflammatory T cells in EAE.Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitis Involvement of the janus kinase/signal transducer and activator of transcription signaling pathway in multiple sclerosis and the animal model of experimental autoimmune encephalomyelitis.Cytokine-regulated neutrophil recruitment is required for brain but not spinal cord inflammation during experimental autoimmune encephalomyelitis.GM-CSF-neuroantigen fusion proteins reverse experimental autoimmune encephalomyelitis and mediate tolerogenic activity in adjuvant-primed environments: association with inflammation-dependent, inhibitory antigen presentation.The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque species The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation.IL-23 modulated myelin-specific T cells induce EAE via an IFNγ driven, IL-17 independent pathway.Comparison of a classical Th1 bacteria versus a Th17 bacteria as adjuvant in the induction of experimental autoimmune encephalomyelitis Silencing IFN-γ binding/signaling in astrocytes versus microglia leads to opposite effects on central nervous system autoimmunity.The many faces of Th17 cells STAT4 controls GM-CSF production by both Th1 and Th17 cells during EAE.Th Cell Diversity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.IFN-γ protects from lethal IL-17 mediated viral encephalomyelitis independent of neutrophils.The chemokine receptor CXCR2 and coronavirus-induced neurologic disease.Mechanisms regulating regional localization of inflammation during CNS autoimmunity.Systemic lack of canonical histamine receptor signaling results in increased resistance to autoimmune encephalomyelitis.Modeling the heterogeneity of multiple sclerosis in animals Inflammasome-derived IL-1β regulates the production of GM-CSF by CD4(+) T cells and γδ T cells Highly polarized Th17 cells induce EAE via a T-bet independent mechanism.Autoantibodies to Non-myelin Antigens as Contributors to the Pathogenesis of Multiple Sclerosis.Treatment of experimental autoimmune encephalomyelitis by codelivery of disease associated Peptide and dexamethasone in acetalated dextran microparticles T(H)17 cytokines in autoimmune neuro-inflammation.Experimental autoimmune encephalomyelitis--achievements and prospective advances.Adaptive immune responses in CNS autoimmune disease: mechanisms and therapeutic opportunities.Th17 cells in autoimmune diseases.The contribution of neutrophils to CNS autoimmunity.Cytokine networks in neuroinflammation.Pre-existing central nervous system lesions negate cytokine requirements for regional experimental autoimmune encephalomyelitis development.AMP-Activated Protein Kinase Suppresses Autoimmune Central Nervous System Disease by Regulating M1-Type Macrophage-Th17 Axis.T-bet promotes the accumulation of encephalitogenic Th17 cells in the CNS.IL-12Rβ2 has a protective role in relapsing-remitting experimental autoimmune encephalomyelitis.T-bet Expression by Foxp3(+) T Regulatory Cells is Not Essential for Their Suppressive Function in CNS Autoimmune Disease or Colitis.

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EAE mediated by a non-IFN-γ/non-IL-17 pathway.

http://www.wikidata.org/entity/Q34142931

description

2010 nî lūn-bûn

@nan

2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

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2010年論文

@zh-tw

2010年论文

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name

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@ast

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@en

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@nl

type

label

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@ast

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@en

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@nl

prefLabel

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@ast

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

@en

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

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European Journal of Immunology

P1476

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

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P2093

Benjamin M Segal

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Mark A Kroenke

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Stephen W Chensue

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P2860

IL-35 is a novel cytokine with therapeutic effects against collagen-induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells

Mice lacking the MHC class II-associated invariant chain

Defective major histocompatibility complex class II assembly, transport, peptide acquisition, and CD4+ T cell selection in mice lacking invariant chain expression

IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain

Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination

Differential regulation of central nervous system autoimmunity by T(H)1 and T(H)17 cells.

Interleukin-17 mRNA expression in blood and CSF mononuclear cells is augmented in multiple sclerosis.

Th1, Th17, and Th9 effector cells induce experimental autoimmune encephalomyelitis with different pathological phenotypes

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