DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Psoriasis. The EFO term psoriasis was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: psoriasis

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

A Strange, F Capon, CC Spencer, J Knight, ME Weale, MH Allen, A Barton, G Band, C Bellenguez, JG Bergboer, JM Blackwell, E Bramon, SJ Bumpstead, JP Casas, MJ Cork, A Corvin, P Deloukas, A Dilthey, A Duncanson, S Edkins, X Estivill, O Fitzgerald, C Freeman, E Giardina, E Gray, A Hofer, U Hüffmeier, SE Hunt, AD Irvine, J Jankowski, B Kirby, C Langford, J Lascorz, J Leman, S Leslie, L Mallbris, HS Markus, CG Mathew, WH McLean, R McManus, R Mössner, L Moutsianas, AT Naluai, FO Nestle, G Novelli, A Onoufriadis, CN Palmer, C Perricone, M Pirinen, R Plomin, SC Potter, RM Pujol, A Rautanen, E Riveira-Munoz, AW Ryan, W Salmhofer, L Samuelsson, SJ Sawcer, J Schalkwijk, CH Smith, M Ståhle, Z Su, R Tazi-Ahnini, H Traupe, AC Viswanathan, RB Warren, W Weger, K Wolk, N Wood, J Worthington, HS Young, PL Zeeuwen, A Hayday, AD Burden, CE Griffiths, J Kere, A Reis, G McVean, DM Evans, MA Brown, JN Barker, L Peltonen, P Donnelly, RC Trembath

TITLE:

A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1.

JOURNAL:

Nature genetics Nov 2010, Vol 42, pp. 985-90

ABSTRACT:

To identify new susceptibility loci for psoriasis, we undertook a genome-wide association study of 594,224 SNPs in 2,622 individuals with psoriasis and 5,667 controls. We identified associations at eight previously unreported genomic loci. Seven loci harbored genes with recognized immune functions (IL28RA, REL, IFIH1, ERAP1, TRAF3IP2, NFKBIA and TYK2). These associations were replicated in 9,079 European samples (six loci with a combined P < 5 × 10⁻⁸ and two loci with a combined P < 5 × 10⁻⁷). We also report compelling evidence for an interaction between the HLA-C and ERAP1 loci (combined P = 6.95 × 10⁻⁶). ERAP1 plays an important role in MHC class I peptide processing. ERAP1 variants only influenced psoriasis susceptibility in individuals carrying the HLA-C risk allele. Our findings implicate pathways that integrate epidermal barrier dysfunction with innate and adaptive immune dysregulation in psoriasis pathogenesis. PUBMED: 20953190
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