Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis. - Wikidata - awgldk - TriplyDB

Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis.

Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis.

http://www.wikidata.org/entity/Q43205286

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Fate mapping of IL-17-producing T cells in inflammatory responses The immunomodulatory and neuroprotective effects of mesenchymal stem cells (MSCs) in experimental autoimmune encephalomyelitis (EAE): a model of multiple sclerosis (MS)Expression of Ccl11 associates with immune response modulation and protection against neuroinflammation in rats Functional and pathogenic differences of Th1 and Th17 cells in experimental autoimmune encephalomyelitis Selective accumulation of pro-inflammatory T cells in the intestine contributes to the resistance to autoimmune demyelinating disease SJL mice infected with Acanthamoeba castellanii develop central nervous system autoimmunity through the generation of cross-reactive T cells for myelin antigens Chloroquine treatment enhances regulatory T cells and reduces the severity of experimental autoimmune encephalomyelitis The tyrosine phosphatase SHP-1 dampens murine Th17 development.Alternative splicing and transcriptome profiling of experimental autoimmune encephalomyelitis using genome-wide exon arrays.Therapeutic and adverse effects of a non-steroidal glucocorticoid receptor ligand in a mouse model of multiple sclerosis.Kinetics of IFN-γ and IL-17 Production by CD4 and CD8 T Cells during Acute Graft-versus-Host Disease.Autoimmune T cell responses in the central nervous system SLAT/Def6 plays a critical role in the development of Th17 cell-mediated experimental autoimmune encephalomyelitis.LPS-matured CD11c+ bone marrow-derived dendritic cells can initiate autoimmune pathology with minimal injection site inflammation.Regulatory T cell induction during Plasmodium chabaudi infection modifies the clinical course of experimental autoimmune encephalomyelitis.Antigen-specific CD25- Foxp3- IFN-gamma(high) CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17.IL-23 suppresses innate immune response independently of IL-17A during carcinogenesis and metastasis.Optimal attenuation of experimental autoimmune encephalomyelitis by intravenous immunoglobulin requires an intact interleukin-11 receptor.Spontaneous autoimmune dacryoadenitis in aged CD25KO mice Th1 and Th17 cells: adversaries and collaborators Th1, Th17, and Th9 effector cells induce experimental autoimmune encephalomyelitis with different pathological phenotypes Expression and regulation in the brain of the chemokine CCL27 gene locus.Increase in Th17 and T-reg lymphocytes and decrease of IL22 correlate with the recovery phase of acute EAE in rat.Intestinal barrier dysfunction develops at the onset of experimental autoimmune encephalomyelitis, and can be induced by adoptive transfer of auto-reactive T cells.EAE mediated by a non-IFN-γ/non-IL-17 pathway.Discrepancy in CCL2 and CCR2 expression in white versus grey matter hippocampal lesions of Multiple Sclerosis patients.Unlike Th1, Th17 cells mediate sustained autoimmune inflammation and are highly resistant to restimulation-induced cell death A crucial role of IL-17 and IFN-γ during acute rejection of peripheral nerve xenotransplantation in mice.Exacerbation of autoimmune neuro-inflammation in mice cured from blood-stage Plasmodium berghei infection.Progression of relapsing-remitting demyelinating disease does not require increased TCR affinity or epitope spread Clinical associations of serum interleukin-17 in systemic lupus erythematosus.Proinflammatory cytokine gene expression in the stomach correlates with vaccine-induced protection against Helicobacter pylori infection in mice: an important role for interleukin-17 during the effector phase.In vivo Treg suppression assays.Modification of the FoxP3 transcription factor principally affects inducible T regulatory cells in a model of experimental autoimmune encephalomyelitis.Chemokine receptors CCR6 and CXCR3 are necessary for CD4(+) T cell mediated ocular surface disease in experimental dry eye disease.Effects of early IL-17A neutralization on disease induction in a primate model of experimental autoimmune encephalomyelitis.Effector and regulatory T-cell subsets in autoimmunity and tissue inflammation.The Role of Th17 in Neuroimmune Disorders: A Target for CAM Therapy. Part III Tissue-specific expression of B7x protects from CD4 T cell-mediated autoimmunity.Role of IL-17 and Th17 cells in herpes simplex virus-induced corneal immunopathology.

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Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis.

http://www.wikidata.org/entity/Q43205286

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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name

Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

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Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

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type

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Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

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Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

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prefLabel

Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

@en

Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

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JIMMUNOL.181.6.3750

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Journal of Immunology

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Cutting edge: Th1 cells facili ...... autoimmune encephalomyelitis.

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Catherine A Sabatos

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Catriona T Prendergast

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Clement W Z Lau

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David C Wraith

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Melanie D Leech

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Richard A O'Connor

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Stephen M Anderton

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P2860

The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells

The inhibitory cytokine IL-35 contributes to regulatory T-cell function

The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation

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

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

Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis

TGF-beta and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain T(H)-17 cell-mediated pathology.

IL-25 regulates Th17 function in autoimmune inflammation.

Either a Th17 or a Th1 effector response can drive autoimmunity: conditions of disease induction affect dominant effector category.

Inflammatory leukocytes and cytokines in the peptide-induced disease of experimental allergic encephalomyelitis in SJL and B10.PL mice.

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3750-3754

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2008-09-01T00:00:00Z

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23235589

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18768826

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experimental autoimmune encephalomyelitis

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2619513

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