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Published on: March 24, 2015
Association between interferon-γ +874 T/A polymorphism and susceptibility to autoimmune diseases: a meta-analysis
1Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea lyhcgh@korea.ac.kr.
Objective:
The aim of this study was to explore whether the interferon (IFN)-γ +874 T/A polymorphism plays a role in modifying the risk of autoimmune diseases.
Methods:
A meta-analysis was conducted on the association between the IFN-γ +874 T/A polymorphism and autoimmune diseases.
Results:
Eighteen studies with a total of 2952 patients and 3832 controls were included in the meta-analysis. The meta-analysis revealed no association between autoimmune diseases and the IFN-γ +874 T allele in all study subjects (odds ratio (OR)=1.023, 95% confidence interval (CI) = 0.894-1.171, p = 0.738), but stratification by ethnicity indicated an association between the IFN-γ +874 T allele and autoimmune diseases in Latin American subjects (OR = 0.780, 95% CI = 0.629-0.953, p = 0.015). Meta-analysis also revealed an association between autoimmune diseases and the IFN-γ +874 T/A polymorphism in Caucasian and Middle Eastern subjects under a dominant inheritance model (OR = 0.686, 95% CI = 0.489-0.964, p = 0.003; OR = 1.414, 95% CI = 1.102-1.813, p = 0.006). Meta-analysis by autoimmune disease type indicated an association between ITP and the IFN-γ +874 T allele (OR = 1.753, 95% CI = 1.228-2.503, p = 0.002), but not for vasculitis, vitiligo, and auto-immune thyroid disease. Meta-analysis also showed a significant association between the IFN-γ +874 T/A polymorphism and systemic lupus erythematosus (SLE) under the dominant model (OR = 1.668, 95% CI = 1.114-2.497, p = 0.013).
Conclusions:
This meta-analysis indicates that the IFN-γ +874 T/A polymorphism may play a significant role in modifying the risk of autoimmune diseases in Caucasian, Latin American, and Middle Eastern subjects, and in particular shows that the IFN-γ +874 T/A polymorphism is associated with increased genetic susceptibility to idiopathic thrombocytopenic purpura and SLE.
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