Association of NFKB1 -94ins/delATTG promoter polymorphism with susceptibility to autoimmune and inflammatory diseases: a meta-analysis

Tissue Antigens. 2011 Jan;77(1):9-17. doi: 10.1111/j.1399-0039.2010.01559.x. Epub 2010 Sep 6.

Abstract

The aim of our study is to assess the association of NFKB1 -94ins/delATTG promoter polymorphism with autoimmune and inflammatory diseases using a meta-analysis. We surveyed the studies on the association of NFKB1 -94ins/delATTG promoter polymorphism with autoimmune and inflammatory diseases. Meta-analysis was performed for genotypes DD vs WW, WD vs WW, DD vs WW + WD, WD + DD vs WW, and D allele vs W allele in a fixed/random effect model. Seventeen studies (7312 cases and 6193 controls) were identified. When all groups were pooled, we found no association between NFKB1 -94ins/delATTG promoter polymorphism and autoimmune and inflammatory diseases. In ethnic subgroup analyses, we found no association between NFKB1 -94ins/delATTG promoter polymorphism and autoimmune and inflammatory diseases in the Caucasian population. However, an association of NFKB1 -94ins/delATTG promoter polymorphism with autoimmune and inflammatory diseases was found in the Asian population [D vs W: odds ratio (OR) = 0.87, 95% confidence interval (CI) = 0.77-0.99, P = 0.03; WD + DD vs WW: OR = 0.79, 95% CI = 0.65-0.95, P = 0.01; DD vs WW + WD: OR = 0.92, 95% CI = 0.73-1.16, P = 0.11; DD vs WW: OR = 0.80, 95% CI = 0.62-1.03, P = 0.09; WD vs WW: OR = 0.78, 95% CI = 0.65-0.95, P = 0.01]. In disease subgroup analyses, we found no association between NFKB1 -94ins/delATTG promoter polymorphism and inflammatory bowel disease, ankylosing spondylitis and Graves' disease. This meta-analysis suggests a possible association between NFKB1 -94ins/delATTG promoter polymorphism and certain autoimmune and inflammatory diseases in the Asian population, but not in the Caucasian population. This finding demands further investigation.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asian People
  • Autoimmune Diseases / genetics*
  • Gene Deletion
  • Genetic Predisposition to Disease*
  • Humans
  • Inflammation / genetics
  • NF-kappa B p50 Subunit / genetics*
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic*
  • Spondylitis, Ankylosing / genetics*
  • White People

Substances

  • NF-kappa B p50 Subunit
  • NFKB1 protein, human