4.2 Article

CD226 Gly307Ser association with multiple autoimmune diseases: A meta-analysis

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HUMAN IMMUNOLOGY
卷 74, 期 2, 页码 249-255

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2012.10.009

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  1. Nature Science Foundation of China [30771227]

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Background: Recently, there has been increasing evidence shown that a non-synonymous exchange (Gly307Ser/rs763361) of the CD226 gene on chromosome 18q22 is linked to several autoimmune diseases (ADs) including type 1 diabetes (T1D), celiac disease (CED), rheumatoid arthritis (RA), multiple sclerosis (MS), Grave's disease, Wegener's granulomatosis (WG), psoriasis, and primary sicca syndrome (pSS). Taking into consideration that different autoimmune diseases may share some common pathogenic pathways and in order to assess the overall relationship between CD226 Gly307Ser (rs763361) polymorphism and multiple autoimmune diseases, we performed this meta-analysis. Method: All eligible case-control studies were searched in the US National Library of Medicine's PubMed and Embase database. Crude odds ratios (OR) with 95% confidence intervals (CI) were conducted to assess the association. Results: 7876 cases and 8558 controls from 7 published studies which were selected from 149 articles identified by a search of the US National Library of Medicine's PubMed and Embase databases for the period up to 25th April 2012. The total OR for ADs associated with the T allele was 1.19 (95%CI = 1.12-1.27) by random effects model. Significantly increased risks were also observed in the South American (OR=1.72, 95%CI = 1.34-2.20), Asian (OR=1.46, 95%CI = 1.01-2.10), and European (OR=1.29, 95%CI = 1.07-1.58). Similarly, significant associations were observed in two genetic models (OR=1.41, 95%CI = 1.23-1.62 in a codominant model; OR=1.33, 95%CI = 1.18-1.50 in a recessive model). Conclusion: This meta-analysis provided evidence that CD226 Gly307Ser (rs763361) is significantly associated with the risk of multiple autoimmune diseases. (C) 2012 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

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