Meta Gene | 2019

Association between CD247 gene rs2056626 polymorphism and the risk of systemic sclerosis: Evidence from a systematic review and Bayesian hierarchical meta-analysis

 
 
 
 
 
 
 

Abstract


Abstract Background Systemic sclerosis (SSc) is an autoimmune fibrotic disease, in which the genetics has been implicated in its etiopathogenesis. The rs2056626 polymorphisms in CD247 gene, which encodes the T cell receptor zeta subunit, has been identified as one of the susceptibility loci for SSc. A number of studies have addressed to this association; nonetheless, inconsistent results confer the necessity to conduct meta-analysis in order to achieve a more precise comprehension of the subject. Methods We searched PubMed and Scopus databases to retrieve relevant studies up to November 2018. The extracted data were statistically analyzed using hierarchical Bayesian and traditional meta-analysis methods and the association strength was estimated by pooled odds ratios (ORs) or log (OR) with 95% confidence/credible interval, respectively. Results Four studies containing 2205 cases and 2686 healthy controls met our inclusion criteria. Our pooled classical meta-analysis revealed no significant effect of rs2056626 on SSc risk under allelic (OR\u202f=\u202f0.913, 95% CI\u202f=\u202f0.827–1.009, P\u202f=\u202f.076), homozygous (OR\u202f=\u202f0.832, 95% CI\u202f=\u202f0.510–1.356, P\u202f=\u202f.460), heterozygous (OR\u202f=\u202f0.846, 95% CI\u202f=\u202f0.647–1.105, P\u202f=\u202f.220), dominant (OR\u202f=\u202f0.840, 95% CI\u202f=\u202f0.620–1.136, P\u202f=\u202f.258) and recessive (OR\u202f=\u202f0.883, 95% CI\u202f=\u202f0.617–1.263, P\u202f=\u202f.495) models. Further Bayesian hierarchical analysis indicated lack of significant associations in all models. Conclusion Exerting the Bayesian meta-analysis as a powerful strategy to pool the data, the rs2056626 polymorphism may not be a predisposing factor for the risk of SSc.

Volume 22
Pages 100613
DOI 10.1016/j.mgene.2019.100613
Language English
Journal Meta Gene

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