Association Between the Interferon-γ +874 T/A Polymorphism and the Risk and Clinical Manifestations of Systemic Lupus Erythematosus: A Preliminary Study

Shanshan Liu, Ju Li, Yongsheng Li, Yan Liu, Kai Wang, Wenyou Pan Department of Rheumatology, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huaian, People’s Republic of ChinaCorrespondence: Shanshan LiuDepartment of Rheumatology, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huaian, People’s Republic of ChinaEmail drshanshanliu@163.comBackground: Interferon-gamma (IFN-γ) is a pivotal cytokine involved in the development of systemic lupus erythematosus (SLE). The IFN-γ +874 T/A polymorphism has been shown to be related to the susceptibility to SLE in other races, but this has not been investigated in the Chinese Han population.Methods: We designed this study to interpret the potential correlation between this polymorphism and SLE risk in a Chinese Han population. We included 374 SLE patients and 405 controls in this study. Odds ratios and relevant 95% confidence intervals were figured out to evaluate the potential strength of the association.Results: Data revealed that the IFN-γ +874 T/A polymorphism showed an association with an enhanced risk of SLE in this Chinese Han population. TA or TA +AA genotype carriers showed an increased risk of developing SLE. Subgroup analyses found that this polymorphism elevated the risk of SLE among females. Additionally, this polymorphism was associated with clinical manifestations of SLE including lupus nephritis, proteinuria, anti-dsDNA antibodies, anti-Sm antibodies, and SLICC/ACR damage index. Furthermore, we conducted a meta-analysis and found that this polymorphism was associated with the risk of SLE, especially among Asians.Conclusion: Totally, this study detects that the IFN-γ +874 T/A polymorphism is related to the risk and clinical manifestations of SLE in a Chinese Han population.Keywords: interferon-gamma, systemic lupus erythematosus, case–control study, +874 T/A polymorphism