PT  - JOURNAL ARTICLE
AU  - John Bowes
AU  - Pauline Ho
AU  - Edw Flynn
AU  - Faisal Ali
AU  - Helena Marzo-Ortega
AU  - Laura C Coates
AU  - Rich B Warren
AU  - Ross McManus
AU  - Anthony W Ryan
AU  - David Kane
AU  - Eleanor Korendowych
AU  - Neil McHugh
AU  - Oliver FitzGerald
AU  - Jonathon Packham
AU  - Ann W Morgan
AU  - Ian N Bruce
AU  - Anne Barton
TI  - Comprehensive assessment of rheumatoid arthritis susceptibility loci in a large psoriatic arthritis cohort
AID  - 10.1136/annrheumdis-2011-200802
DP  - 2012 Feb 01
TA  - Annals of the Rheumatic Diseases
PG  - annrheumdis-2011-200802
4099  - http://ard.bmj.com/content/early/2012/02/09/annrheumdis-2011-200802.short
4100  - http://ard.bmj.com/content/early/2012/02/09/annrheumdis-2011-200802.full
AB  - Objective A number of rheumatoid arthritis (RA) susceptibility genes have been identified in recent years. Given the overlap in phenotypic expression of synovial joint inflammation between RA and psoriatic arthritis (PsA), the authors explored whether RA susceptibility genes are also associated with PsA. Methods 56 single nucleotide polymorphisms (SNPs) mapping to 41 genes previously reported as RA susceptibility loci were selected for investigation. PsA was defined as an inflammatory arthritis associated with psoriasis and subjects were recruited from the UK and Ireland. Genotyping was performed using the Sequenom MassArray platform and frequencies compared with data derived from large UK control collections. Results Significant evidence for association with susceptibility to PsA was found toa SNP mapping to the REL (rs13017599, ptrend=5.2×104) gene, while nominal evidence for association (ptrend<0.05) was found to seven other loci including PLCL2 (rs4535211, p=1.7×10−3); STAT4 (rs10181656, p=3.0×10−3) and the AFF3, CD28, CCL21, IL2 and KIF5A loci. Interestingly, three SNPs demonstrated opposite effects to those reported for RA. Conclusions The REL gene, a key modulator of the NFκB pathway, is associated with PsA but the allele conferring risk to RA is protective in PsA suggesting that there are fundamental differences in the aetiological mechanisms underlying these two types of inflammatory arthritis.