Association between cytotoxic T lymphocyte associated antigen-4 gene polymorphism and ankylosing spondylitis susceptibility: a meta-analysis
10.3760/cma.j.issn.1007-7480.2017.08.009
- VernacularTitle:强直性脊柱炎与细胞毒性T细胞相关抗原-4基因多态性的Meta分析
- Author:
Xiaomin LIU
;
Yinhe CHEN
- Keywords:
Spondylitis,ankylosing;
T-lymphocyte,cytotoxic;
Polymorphism,single nucleotide;
Meta-analysis
- From:Chinese Journal of Rheumatology
2017;21(8):547-552
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the association between cytotoxic T lymphocyte associated antigen-4 (CTLA-4) gene polymorphism and susceptibility to ankylosing spondylitis (AS). Methods The case-control studies from Chinese Biomedical Database, Chinese National Knowledge Infrastructure, Wanfang, Weipu, PubMed, Cochrane Library, OvidSP, Wiley Online Library, Elsevier Science Direct, Springer Link databases for the association of CTLA-4 gene polymorphism with AS. The association strength was assessed with chi-squared test by Stata 12.0 software. Results Seven references of CTLA-4 gene +49A/G (rs231775) polymorphism were enrolled which included 1119 AS patients and 995 controls (healthy subjects or non-AS patients), which showed that there were no statistical difference between AS and control groups under recessive, dominant, co-dominant, additive and allele gene models. Five references of CTLA-4 gene-318C/T (rs5742909) polymorphism were enrolled which included 635 AS patients and 512 controls, which showed that there were no statistical difference between AS and control groups under recessive and additive gene models; however, there were statistical difference between AS and control groups under dominant model [ OR=1.651, 95%CI (1.052, 2.590), P=0.029], co-dominant model [OR=0.621, 95%CI (0.403, 0.957), P=0.031] and allele model [OR=1.587, 95%CI (1.068, 2.357), P=0.022]. Conclusion The meta analysis reveal that CTLA-4 gene rs231775 single nucleotide polymorphism is not associated with the susceptibility to AS; rs5742909 SNP is associated with the susceptibility to AS, which suggests that C→T mutation increases the risk of AS.
