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Defective tumor necrosis factor release from Crohn's disease macrophages in response to Toll-like receptor activation: relationship to phenotype and genome-wide association susceptibility loci.

Gavin W Sewell | Farooq Z Rahman | Adam P Levine | Luke Jostins | Philip J Smith | Ann P Walker | Stuart L Bloom | Anthony W Segal | Andrew M Smith
Inflammatory bowel diseases | 2012

Recent work provides evidence of a failure of acute inflammation in Crohn's disease (CD), and suggests that the primary defect operates at the level of the macrophage and cytokine release. Here we extend the characterization of the innate immune defect in CD by investigating the macrophage response to Toll-like receptor (TLR) agonists and assess potential links between genome-wide association study (GWAS) susceptibility loci, disease phenotype, and therapeutic regimens on tumor necrosis factor α (TNF) release.

Pubmed ID: 22434667

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Associated grants

  • Agency: Department of Health, United Kingdom
    Id: 482
  • Agency: Medical Research Council, United Kingdom
    Id: G0902022
  • Agency: Wellcome Trust, United Kingdom

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NCTC clone 929 (tool)

RRID:CVCL_0462

Cell line NCTC clone 929 is a Spontaneously immortalized cell line with a species of origin Mus musculus

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