Title: The role of the Toll receptor pathway in susceptibility to inflammatory bowel diseases
Authors: De Jager, P. L ×
Franchimont, D
Waliszewska, A
Bitton, A
Cohen, A
Langelier, D
Belaiche, J
Vermeire, Severine
Farwell, L
Goris, An
Libioulle, C
Jani, N
Dassopoulos, T
Bromfield, G. P
Dubois, Bénédicte
Cho, J. H
Brant, S. R
Duerr, R. H
Yang, Hu
Rotter, J. I
Silverberg, M. S
Steinhart, A. H
Daly, M. J
Podolsky, D. K
Louis, E
Hafler, D. A
Rioux, J. D #
Issue Date: Jul-2007
Publisher: Nature publishing group
Series Title: Genes and immunity vol:8 issue:5 pages:387-397
Abstract: The intestinal flora has long been thought to play a role either in initiating or in exacerbating the inflammatory bowel diseases (IBD). Host defenses, such as those mediated by the Toll-like receptors (TLR), are critical to the host/pathogen interaction and have been implicated in IBD pathophysiology. To explore the association of genetic variation in TLR pathways with susceptibility to IBD, we performed a replication study and pooled analyses of the putative IBD risk alleles in NFKB1 and TLR4, and we performed a haplotype-based screen for association to IBD in the TLR genes and a selection of their adaptor and signaling molecules. Our genotyping of 1539 cases of IBD and pooled analysis of 4805 cases of IBD validates the published association of a TLR4 allele with risk of IBD (odds ratio (OR): 1.30, 95% confidence interval (CI): 1.15 - 1.48; P = 0.00017) and Crohn's disease (OR: 1.33, 95% CI: 1.16 - 1.54; P = 0.000035) but not ulcerative colitis. We also describe novel suggestive evidence that TIRAP (OR: 1.16, 95% CI: 1.04 - 1.30; P = 0.007) has a modest effect on risk of IBD. Our analysis, therefore, offers additional evidence that the TLR4 pathway - in this case, TLR4 and its signaling molecule TIRAP - plays a role in susceptibility to IBD.
ISSN: 1466-4879
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Research Group Experimental Neurology
Translational Research in GastroIntestinal Disorders
Laboratory for Neuroimmunology
× corresponding author
# (joint) last author

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