4.2 Article

STAT4 gene influences genetic predisposition to ulcerative colitis but not Crohn's disease in the Spanish population: A replication study

期刊

HUMAN IMMUNOLOGY
卷 71, 期 5, 页码 515-519

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2010.02.005

关键词

Signal transducer and activator of transcription 4 (STAT4) gene; Inflammatory bowel disease; Crohn's disease; Ulcerative colitis; Genetic association study

资金

  1. Junta de Andalucia [CTS-1180]
  2. COLFUTURO
  3. Institut de Salud Carlos III [PFIS - FI09/00544]
  4. [SAF2006-00398]

向作者/读者索取更多资源

Recently, the signal transducer and activator of transcription 4 (STAT4) gene has been associated with multiple autoimmune diseases. Interestingly, a recent work showed that the T allele of the rs7574865 STAT4 SNP was associated with inflammatory bowel disease (IBD) in a Spanish population. The aim of the present study was to reevaluate the role of the STAT4 rs7574865 polymorphism on IBD. The present case-control study included 498 Crohn's disease (CD) patients, 402 ulcerative colitis (DC) patients, and 1296 healthy matched controls. Genotyping was performed using a PCR system with a pre-developed TaqMan allelic discrimination assay for the rs7574865 STAT4 SNP. Moreover, a meta-analysis was performed with the previous work in a Spanish population and the current study, including a final sample size of 1574 IBD patients (820 with CD and 754 with UC) and 2012 healthy controls. No evidence of association was found for the current case-control study (CD: p = 0.23, OR = 0.9,95% CI = 0.75-1.1; UC: p = 0.17, OR = 1.14, 95% CI = 0.95-1.38). However, the meta-analysis showed that the STAT4 rs7574865 T allele was significantly associated with susceptibility to UC (p = 0.012 pooled; OR = 1.20, 95% CI = 1.04-1.39) but not CD (p = 0.71 pooled; OR = 0.93, 95% CI = 0.65-1.34). Our data suggest that the rs7574865 STAT4 SNP is a genetic susceptibility variant for DC but not CD in the Spanish population. (C) 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

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