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Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease
It is suggested that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn’s disease that can now be further investigated.
Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease
The results strongly confirm 11 previously reported loci and provide genome-wide significant evidence for 21 additional loci, including the regions containing STAT3, JAK2, ICOSLG, CDKAL1 and ITLN1, which offer promise for informed therapeutic development.
Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci
A meta-analysis of six Crohn's disease genome-wide association studies and a series of in silico analyses highlighted particular genes within these loci implicated functionally interesting candidate genes including SMAD3, ERAP2, IL10, IL2RA, TYK2, FUT2, DNMT3A, DENND1B, BACH2 and TAGAP.
CARD15/NOD2 mutational analysis and genotype-phenotype correlation in 612 patients with inflammatory bowel disease.
The mutational analyses of CARD15 in 453 patients with CD, including 166 sporadic and 287 familial cases, 159 patients with ulcerative colitis (UC), and 103 healthy control subjects provide tools for a DNA-based test of susceptibility and for genetic counseling in inflammatory bowel disease.
Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47
A meta-analysis of six ulcerative colitis genome-wide association study datasets found many candidate genes that provide potentially important insights into disease pathogenesis, including IL1R2, IL8RA-IL8RB, IL7R, IL12B, DAP, PRDM1, JAK2, IRF5, GNA12 and LSP1.
Consensus guidelines of ECCO/ESPGHAN on the medical management of pediatric Crohn's disease.
CARD15 mutations in Blau syndrome
Findings indicate that, in addition to Crohn disease, CARD15 is involved in the susceptibility to a second granulomatous disorder.
The NLR gene family: a standard nomenclature.
A critical role for peptidoglycan N-deacetylation in Listeria evasion from the host innate immune system
- I. Boneca, O. Dussurget, S. Girardin
- BiologyProceedings of the National Academy of Sciences
- 16 January 2007
Results reveal that PG N-deacetylation is a highly efficient mechanism used by Listeria to evade innate host defenses and indicates that deacetylase genes in other pathogenic bacteria could be a general mechanism used to evade the host innate immune system.
Crohn disease--associated adherent-invasive E. coli bacteria target mouse and human Peyer's patches via long polar fimbriae.
- B. Chassaing, Nathalie Rolhion, A. Darfeuille‐Michaud
- Biology, MedicineThe Journal of clinical investigation
- 1 March 2011
LPF is identified as a key factor for AIEC to target PPs, which could be the missing link between AIEC colonization and the presence of early lesions in the PPs of CD patients.