Department of Endocrinology and Metabolism, Binzhou Medical University Hospital, 661 Second Huanghe Road, Binzhou 256603, China.
Department of Internal Medicine, Linzi District People's Hospital, No. 139 Huangong Road, Zibo 255400, China.
Mediators Inflamm. 2020 Apr 28;2020:7825072. doi: 10.1155/2020/7825072. eCollection 2020.
Some certain genetic polymorphisms have been considered to implicate in the pathogenesis and progression of autoimmune diseases and may predispose to an early stage of general autoimmune susceptibility. Recent studies have been conducted to investigate the association between macrophage migration inhibitory factor- (MIF-) 173G/C gene polymorphism and autoimmune diseases; however, the results were not exactly identical. In the present study, a systematic review and meta-analysis of case-control studies was performed to estimate the relationship. A comprehensive search of PubMed, Ebsco, EMbase, WanFang databases and CNKI was done. Odds ratio (ORs) and corresponding 95% confidence intervals (CIs) were combined to pool the effect size. The publication bias was examined by Begg's funnel plots and Egger's test. RevMan 5.3 and STATA 12.0 software were used for statistical processing. 23 papers were included, and the results revealed that MIF-173G/C was significantly associated with an increased risk of autoimmune diseases in five genetic models (recessive genetic model: OR = 1.95, 95% CI: 1.52-2.50; dominant genetic model: OR = 1.35, 95% CI: 1.24-1.46; allele model: OR = 1.32, 95% CI: 1.23-1.41; homozygote model: OR = 1.92, 95% CI: 1.57-2.35; heterozygote model: OR = 4.92, 95% CI: 4.03-6.02), whether in Asia, Europe, or North America. Furthermore, subgroup analysis showed an increasing risk in rheumatoid arthritis (RA), ulcerative colitis (UC), Crohn's disease (CD), atopic dermatitis (AD), Henoch-Schonlein purpura (HSP), and Henoch-Schonlein purpura nephritis (HSPN), but it was not related to the susceptibility of autoimmune hepatitis (AIH). Therefore, it could be considered that MIF-173G/C polymorphism could increase the susceptibility of autoimmune diseases, while there may be the discrepancy of disease entity.
一些特定的遗传多态性被认为与自身免疫性疾病的发病机制和进展有关，并且可能使机体易患一般性自身免疫的早期阶段。最近的研究已经对巨噬细胞移动抑制因子（MIF）-173G/C 基因多态性与自身免疫性疾病之间的关系进行了调查；然而，结果并不完全一致。本研究通过系统综述和病例对照研究的荟萃分析来评估这种相关性。通过全面搜索 PubMed、Ebsco、EMbase、万方数据库和中国知网来进行搜索。使用比值比（OR）和相应的 95％置信区间（CI）来合并效应大小。通过 Begg 漏斗图和 Egger 检验来检查发表偏倚。RevMan 5.3 和 STATA 12.0 软件用于统计处理。纳入 23 篇文献，结果显示 MIF-173G/C 与五种遗传模型下自身免疫性疾病的风险增加显著相关（隐性遗传模型：OR=1.95，95％CI：1.52-2.50；显性遗传模型：OR=1.35，95％CI：1.24-1.46；等位基因模型：OR=1.32，95％CI：1.23-1.41；纯合子模型：OR=1.92，95％CI：1.57-2.35；杂合子模型：OR=4.92，95％CI：4.03-6.02），无论在亚洲、欧洲还是北美洲。此外，亚组分析显示类风湿关节炎（RA）、溃疡性结肠炎（UC）、克罗恩病（CD）、特应性皮炎（AD）、过敏性紫癜（HSP）和过敏性紫癜肾炎（HSPN）的风险增加，但与自身免疫性肝炎（AIH）的易感性无关。因此，可以认为 MIF-173G/C 多态性可能会增加自身免疫性疾病的易感性，而疾病实体可能存在差异。
