Association of IL-23R gene rs7517847 T>G SNP and susceptibility to systemic lupus erythematosus: A systematic review and meta-analysis
(ندگان)پدیدآور
Imani, DanyalRezaei, RamazanPoorsheikhani, ArashAlizadeh, ShahabMahmoudi, Mahdiنوع مدرک
TextMeta-Analysis
زبان مدرک
Englishچکیده
Previous articles have evaluated the association between IL-23R gene rs7517847 T>G SNP and systemic lupus erythematosus (SLE). Nevertheless, the results of these studies have been inconclusive. The current study is a meta-analysis that assesses the association between IL-23R gene rs7517847 T>G SNP and SLE susceptibility. Literature searches of Medline, Web of Science, and EMBASE databases were performed to recognize all eligible studies published before August, 2016, and the search was updated in July, 2017. The identified studies were independently reviewed by two authors for eligibility based on inclusion criteria. Odds ratios (ORs) and 95% confidence intervals (CIs) were applied to assess the strength of association in the allelic model, dominant model, recessive model, heterozygotes contrast, and homozygotes contrast. Because evidence of heterogeneity was detected across the studies, the data was pooled using a random-effects model. A sum of four case-control studies with 1348 SLE patients and 1754 healthy subjects were considered in this study. In the combined analysis, no significant association between the IL-23R gene rs7517847 T>G SNP and SLE disease risk was found in any of the genetic models (dominant model: OR = 0.95, 95% CI = 0.72-1.18; allelic model: OR = 1.08, 95% CI = 0.95-1.21; recessive model: OR = 1.13, 95% CI = 0.80-1.46; TG vs. TT: OR = 0.86, 95% CI = 0.63-1.08; and GG vs. TT: OR = 1.20, 95% CI = 0.81-1.60). Moreover, no publication bias was observed in any genetic models (G SNP and systemic lupus erythematosus (SLE). Nevertheless, the results of these studies have been inconclusive. The current study is a meta-analysis that assesses the association between IL-23R gene rs7517847 T>G SNP and SLE susceptibility. Literature searches of Medline, Web of Science, and EMBASE databases were performed to recognize all eligible studies published before August, 2016, and the search was updated in July, 2017. The identified studies were independently reviewed by two authors for eligibility based on inclusion criteria. Odds ratios (ORs) and 95% confidence intervals (CIs) were applied to assess the strength of association in the allelic model, dominant model, recessive model, heterozygotes contrast, and homozygotes contrast. Because evidence of heterogeneity was detected across the studies, the data was pooled using a random-effects model. A sum of four case-control studies with 1348 SLE patients and 1754 healthy subjects were considered in this study. In the combined analysis, no significant association between the IL-23R gene rs7517847 T>G SNP and SLE disease risk was found in any of the genetic models (dominant model: OR = 0.95, 95% CI = 0.72-1.18; allelic model: OR = 1.08, 95% CI = 0.95-1.21; recessive model: OR = 1.13, 95% CI = 0.80-1.46; TG vs. TT: OR = 0.86, 95% CI = 0.63-1.08; and GG vs. TT: OR = 1.20, 95% CI = 0.81-1.60). Moreover, no publication bias was observed in any genetic models (G SNP and SLE susceptibility. Literature searches of Medline, Web of Science, and EMBASE databases were performed to recognize all eligible studies published before August, 2016, and the search was updated in July, 2017. The identified studies were independently reviewed by two authors for eligibility based on inclusion criteria. Odds ratios (ORs) and 95% confidence intervals (CIs) were applied to assess the strength of association in the allelic model, dominant model, recessive model, heterozygotes contrast, and homozygotes contrast. Because evidence of heterogeneity was detected across the studies, the data was pooled using a random-effects model. A sum of four case-control studies with 1348 SLE patients and 1754 healthy subjects were considered in this study. In the combined analysis, no significant association between the IL-23R gene rs7517847 T>G SNP and SLE disease risk was found in any of the genetic models (dominant model: OR = 0.95, 95% CI = 0.72-1.18; allelic model: OR = 1.08, 95% CI = 0.95-1.21; recessive model: OR = 1.13, 95% CI = 0.80-1.46; TG vs. TT: OR = 0.86, 95% CI = 0.63-1.08; and GG vs. TT: OR = 1.20, 95% CI = 0.81-1.60). Moreover, no publication bias was observed in any genetic models (G SNP and SLE disease risk was found in any of the genetic models (dominant model: OR = 0.95, 95% CI = 0.72-1.18; allelic model: OR = 1.08, 95% CI = 0.95-1.21; recessive model: OR = 1.13, 95% CI = 0.80-1.46; TG vs. TT: OR = 0.86, 95% CI = 0.63-1.08; and GG vs. TT: OR = 1.20, 95% CI = 0.81-1.60). Moreover, no publication bias was observed in any genetic models (p> 0.05). First, this study was based on unadjusted ORs. Second, the number of included case-control articles was small. Third, only published English language studies were imported to this meta-analysis. The current meta-analysis suggests that the IL-23R gene rs7517847 T>G SNP might not be related with risk of SLE. More studies are essential to confirm these results. No association was found between the IL-23R gene rs7517847 T>G SNP and SLE risk.
کلید واژگان
interleukin-23RPolymorphism
SLE
Meta-analysis
Immunology
شماره نشریه
1تاریخ نشر
2018-01-011396-10-11
ناشر
Rheumatology Research in cooperation with eJournalPlusسازمان پدید آورنده
Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, IranRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran
Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran




