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    • مشاهده مورد
    •   صفحهٔ اصلی
    • نشریات انگلیسی
    • Rheumatology Research
    • Volume 3, Issue 1
    • مشاهده مورد
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    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, Mahdi
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    نوع مدرک
    Text
    Meta-Analysis
    زبان مدرک
    English
    نمایش کامل رکورد
    چکیده
    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-23R
    Polymorphism
    SLE
    Meta-analysis
    Immunology

    شماره نشریه
    1
    تاریخ نشر
    2018-01-01
    1396-10-11
    ناشر
    Rheumatology Research in cooperation with eJournalPlus
    سازمان پدید آورنده
    Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
    Rheumatology 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

    شاپا
    2476-5856
    URI
    https://dx.doi.org/10.22631/rr.2017.69997.1036
    http://www.rheumres.org/article_50580.html
    https://iranjournals.nlai.ir/handle/123456789/56319

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