TLR5 is not required for flagellin-mediated exacerbation of DSS colitis. - Wikidata - wikimedia - TriplyDB

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

http://www.wikidata.org/entity/Q50053000

about

Role of commensal gut bacteria in inflammatory bowel diseases Epithelial IL-23R Signaling Licenses Protective IL-22 Responses in Intestinal Inflammation Insulin modulates the inflammatory granulocyte response to streptococci via phosphatidylinositol 3-kinase.Microbial ecology of the murine gut associated with the development of dextran sodium sulfate-induced colitis.TLR5 activation induces secretory interleukin-1 receptor antagonist (sIL-1Ra) and reduces inflammasome-associated tissue damage.Basic and translational understandings of microbial recognition by toll-like receptors in the intestine.A non-synonymous coding variant (L616F) in the TLR5 gene is potentially associated with Crohn's disease and influences responses to bacterial flagellin Interrelatedness between dysbiosis in the gut microbiota due to immunodeficiency and disease penetrance of colitis.Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges Toll-like receptor 5 engagement induces interleukin-17C expression in intestinal epithelial cells Regulatory T-cell therapy for inflammatory bowel disease: more questions than answers.ATP conditions intestinal epithelial cells to an inflammatory state that promotes components of DC maturation.Influence of Intestinal Microbiota Transplantation and NleH Expression on Citrobacter rodentium Colonization of Mice.Emerging Mechanisms of Innate Immunity and Their Translational Potential in Inflammatory Bowel Disease.

P2860

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P2860

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

http://www.wikidata.org/entity/Q50053000

description

2010 nî lūn-bûn

@nan

2010年の論文

@ja

2010年学术文章

@wuu

2010年学术文章

@zh

2010年学术文章

@zh-cn

2010年学术文章

@zh-hans

2010年学术文章

@zh-my

2010年学术文章

@zh-sg

2010年學術文章

@yue

2010年學術文章

@zh-hant

name

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@en

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@nl

type

label

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@en

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@nl

prefLabel

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@en

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@nl

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P1433

Inflammatory Bowel Diseases

P1476

TLR5 is not required for flagellin-mediated exacerbation of DSS colitis.

@en

P2093

Arnawaz Kifayet

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

Gijs Hardenberg

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

Megan E Himmel

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

Paige A J Wark

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

Sabine M Ivison

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

P2860

Antibody to Saccharomyces cerevisiae (bakers' yeast) in Crohn's disease

On the use of haplotype phylogeny to detect disease susceptibility loci

Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease

Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis

Two nonadjacent regions in enteroaggregative Escherichia coli flagellin are required for activation of toll-like receptor 5.

Innate and adaptive immune responses related to IBD pathogenesis.

Epithelial toll-like receptor 5 is constitutively localized in the mouse cecum and exhibits distinctive down-regulation during experimental colitis.

Anatomical basis of tolerance and immunity to intestinal antigens.

Pathophysiological role of Toll-like receptor 5 engagement by bacterial flagellin in colonic inflammation.

The fundamental basis of inflammatory bowel disease.

P304

401-409

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scholarly article

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10.1002/IBD.21097

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3

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16

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Megan K Levings

Theodore S Steiner

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2010-03-01T00:00:00Z

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26831893

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19774646

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P921

Toll-like receptor