4.7 Article

Confirmation of TNIP1 and IL23A as susceptibility loci for psoriatic arthritis

Journal

ANNALS OF THE RHEUMATIC DISEASES
Volume 70, Issue 9, Pages 1641-1644

Publisher

B M J PUBLISHING GROUP
DOI: 10.1136/ard.2011.150102

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Funding

  1. NIHR Manchester Biomedical Research Centre
  2. NIHR Leeds Musculoskeletal Biomedical Research Unit
  3. Arthritis Research UK [17552]
  4. European Community
  5. Arthritis Research UK
  6. Wellcome Trust [076113, 085475]
  7. MRC [G1001799] Funding Source: UKRI
  8. Medical Research Council [G1001799] Funding Source: researchfish

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Objectives To investigate a shared genetic aetiology for skin involvement in psoriasis and psoriatic arthritis (PsA) by genotyping single-nucleotide polymorphisms (SNPs), reported to be associated in genome-wide association studies of psoriasis, in patients with PsA. Methods SNPs with reported evidence for association with psoriasis were genotyped in a PsA case and control collection from the UK and Ireland. Genotype and allele frequencies were compared between PsA cases and controls using the Armitage test for trend. Results Seven SNPs mapping to the IL1RN, TNIP1, TNFAIP3, TSC1, IL23A, SMARCA4 and RNF114 genes were successfully genotyped. The IL23A and TNIP1 genes showed convincing evidence for association (rs2066808, p = 9.1 x 10(-7); rs17728338, p = 3.5 x 10(-5), respectively) whilst SNPs mapping to the TNFAIP3, TSC1 and RNF114 genes showed nominal evidence for association (rs610604, p = 0.03; rs1076160, p = 0.03; rs495337, p = 0.0025). No evidence for association with IL1RN or SMARCA4 was found but the power to detect association was low. Conclusions SNPs mapping to previously reported psoriasis loci show evidence for association to PSA, thus supporting the hypothesis that the genetic aetiology of skin involvement is the same in both PsA and psoriasis.

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