Mouse IBD models reveal distinct pathogenic and protective roles of MyD88 signalling in epithelial cells and leukocytes

Mouse IBD models reveal distinct pathogenic and protective roles of MyD88 signalling in epithelial cells and leukocytes

Bibliografiset tiedot
Päätekijät:	Asquith, M, Boulard, O, Powrie, F, Maloy, K
Aineistotyyppi:	Conference item
Julkaistu:	2010

Samankaltaisia teoksia

Pathogenic and protective roles of MyD88 in leukocytes and epithelial cells in mouse models of inflammatory bowel disease.
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Correction: The MyD88+ Phenotype Is an Adverse Prognostic Factor in Epithelial Ovarian Cancer
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Correction: The MyD88+ Phenotype Is an Adverse Prognostic Factor in Epithelial Ovarian Cancer.
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Pyogenic bacterial infections in humans with MyD88 deficiency.
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Lipopolysaccharide-induced NF-κB nuclear translocation is primarily dependent on MyD88, but TNFα expression requires TRIF and MyD88
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MyD88 is required for protection from lethal infection with a mouse-adapted SARS-CoV.
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MyD88 in macrophages protects against colitis via inhibiting the activation of NLRP3 inflammasome in epithelial cells
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Two human MYD88 variants, S34Y and R98C, interfere with MyD88-IRAK4-myddosome assembly.
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Loss of TLR4 in mouse Müller cells inhibits both MyD88-dependent and -independent signaling.
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3D quantitative imaging of unprocessed live tissue reveals epithelial defense against bacterial adhesion and subsequent traversal requires MyD88.
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Clinical features and outcome of patients with IRAK-4 and MyD88 deficiency.
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MyD88 Mediates Colitis- and RANKL-Induced Microfold Cell Differentiation
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Induction of Hypergammaglobulinemia and Autoantibodies by Salmonella Infection in MyD88-Deficient Mice
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Ischemia-reperfusion lung injury is attenuated in MyD88-deficient mice.
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Evolution of Toll, Spatzle and MyD88 in insects: the problem of the Diptera bias
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MyD88 promotes myoblast fusion in a cell-autonomous manner
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