Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-09

AUTHORS

Francesca Capon, Paola Di Meglio, Joanna Szaub, Natalie J. Prescott, Christina Dunster, Laura Baumber, Kirsten Timms, Alexander Gutin, Victor Abkevic, A. David Burden, Jerry Lanchbury, Jonathan N. Barker, Richard C. Trembath, Frank O. Nestle

ABSTRACT

Psoriasis is an inflammatory skin disorder that is inherited as a multifactorial trait. Genetic analyses have repeatedly identified a primary disease susceptibility locus lying within the major histocompatibility complex (MHC), on chromosome 6p21. A small number of non-MHC susceptibility loci have also been identified. These regions tend to overlap with susceptibility intervals for Crohn's disease and atopic dermatitis, suggesting the possibility that genetic variants affecting inflammatory pathways may contribute to the pathogenesis of multiple disorders. Here, we report a genetic analysis of the interleukin 23 receptor gene (IL23R), which was recently identified as a susceptibility determinant for Crohn's disease. We initially examined the results of a whole-genome association scan, carried out on 318 cases and 288 controls. We observed a significant increase of a non-synonymous substitution (p.Arg381Gln) among controls (P = 0.00036). We validated this finding by extending our cohort to include a further 519 cases and 528 controls. In the overall sample, the frequency of the 381Gln allele was 3.6% in cases and 7% in controls, yielding a P value of 0.00014. Next, we examined genetic variation at the IL12RB1, IL23A and IL12B genes, respectively, encoding the second subunit of the IL23R receptor and the two subunits of its ligand. This analysis identified independent associations for IL12B SNPs rs10045431 (P value for the extended dataset = 0.0001) and rs3212227 (P = 0.036). Altogether, these findings indicate that genes participating in IL23 signalling play a significant role in the pathogenesis of chronic epithelial inflammation. More... »

PAGES

201-206

Journal

TITLE

Human Genetics

ISSUE

2

VOLUME

122

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00439-007-0397-0

DOI

http://dx.doi.org/10.1007/s00439-007-0397-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1034387357

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17587057


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