Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitis - Wikidata - wikimedia - TriplyDB

Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitis

Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitis

http://www.wikidata.org/entity/Q33880465

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Actions of Thyroid Hormone Analogues on Chemokines Stage-Specific Role of Interferon-Gamma in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis Novel Insights and Therapeutics in Multiple Sclerosis Multiple Sclerosis and T Lymphocytes: An Entangled Story Heterogeneity in oligodendroglia: Is it relevant to mouse models and human disease?Neutrophil contribution to spinal cord injury and repair.Preferential Recruitment of Neutrophils into the Cerebellum and Brainstem Contributes to the Atypical Experimental Autoimmune Encephalomyelitis Phenotype.Anti-inflammatory mechanisms of IFN-γ studied in experimental autoimmune encephalomyelitis reveal neutrophils as a potential target in multiple sclerosis.Therapeutic effect of baicalin on experimental autoimmune encephalomyelitis is mediated by SOCS3 regulatory pathway.Distinct T cell signatures define subsets of patients with multiple sclerosis.Opportunities for Translation from the Bench: Therapeutic Intervention of the JAK/STAT Pathway in Neuroinflammatory Diseases.GM-CSF is not essential for experimental autoimmune encephalomyelitis but promotes brain-targeted disease.Influenza infection triggers disease in a genetic model of experimental autoimmune encephalomyelitis.Neutrophils and viral-induced neurologic disease.The contribution of neutrophils to CNS autoimmunity.Analysis of chemokines and receptors expression profile in the myelin mutant taiep rat.T-bet promotes the accumulation of encephalitogenic Th17 cells in the CNS.GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System-Infiltrating Cells, but Is Dispensable for Disease Induction.Cell-specific and region-specific transcriptomics in the multiple sclerosis model: Focus on astrocytes.Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment.

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P2860

Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitis

http://www.wikidata.org/entity/Q33880465

description

2014 nî lūn-bûn

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2014 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2014 թվականի հունիսին 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

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name

Site-specific chemokine expres ...... n autoimmune encephalomyelitis

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Site-specific chemokine expres ...... n autoimmune encephalomyelitis

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Site-specific chemokine expres ...... n autoimmune encephalomyelitis

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Site-specific chemokine expres ...... n autoimmune encephalomyelitis

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JIMMUNOL.1400825

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Journal of Immunology

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Site-specific chemokine expres ...... n autoimmune encephalomyelitis

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P2093

Amanda K Huber

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Benjamin M Segal

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Joshua S Stoolman

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Patrick C Duncker

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P2860

Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria

CXCR7 influences leukocyte entry into the CNS parenchyma by controlling abluminal CXCL12 abundance during autoimmunity

The choroid plexus response to a repeated peripheral inflammatory stimulus.

A protective role for ELR+ chemokines during acute viral encephalomyelitis.

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

Functional specialization of interleukin-17 family members.

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

T-cell properties determine disease site, clinical presentation, and cellular pathology of experimental autoimmune encephalomyelitis

Synchronous synthesis of alpha- and beta-chemokines by cells of diverse lineage in the central nervous system of mice with relapses of chronic experimental autoimmune encephalomyelitis.

IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

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564-570

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scholarly article

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10.4049/JIMMUNOL.1400825

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2

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193

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Benjamin M. Segal

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Patrick C Duncker

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2014-06-13T00:00:00Z

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263131927

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24928987

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4091641

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