Abstract
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.
Highlights
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine mainly released from Th2 cells and macrophages, which can mediate the host response to infection and stress by activating innate and adaptive immune pathways [1, 2]
There was no significant heterogeneity between the migration inhibitory factor- (MIF-)173G/C polymorphism and autoimmune diseases, so the fixed effects model was used for meta-analysis
A functional singlenucleotide polymorphism (SNP) was identified in the untranslated 5′region of MIF gene at position -173 consisting of a G to C transition [39]
Summary
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine mainly released from Th2 cells and macrophages, which can mediate the host response to infection and stress by activating innate and adaptive immune pathways [1, 2]. MIF is encoded by a single gene located on chromosome 22q11.2m, a 12 kD peptide comprising 114 amino acids [3]. It mainly interacts with its receptor CD74 to form a complex with CD44, which can result in the lasted activation of the ERK-MAPK pathway by a Src tyrosine kinase signal transduction. Downstream effects of this pathway include NFκB translocation to the nucleus, upregulation of PLA2 and prostaglandins, and stimulation of the arachidonic acid pathway [4]. Many studies have indicated that MIF-173G/C is associated with the pathogenesis and progression of autoimmune diseases
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