Background Background: Juvenile arthritis (JA) is an umbrella term used to describe the many autoimmune and inflammatory conditions that can develop in children ages 16 and younger. According to the ILAR criteria JA include 7 disease subtypes. It was shown that JA is as a complex trait and some genes are associated with JIA in different populations and subtypes, including macrophage migration inhibitory (MIF) gene. MIF is a lymphokine involved in cell-mediated immunity, immunoregulation, and inflammation. It plays a role in the regulation of macrophage function in host defense through the suppression of anti-inflammatory effects of glucocorticoids.
Objectives The goal of the study was to examine evidence for association of the MIF*-173G>C polymorphism (rs755622) with different clinical variants of JA.
Methods The MIF*-173G>C SNP was studied in 155 children with juvenile arthritis (JA) and 208 healthy individuals, citizens of the Bashkortostan, using real time PCR. Statistical analysis was performed in Statistica v. 6.0 and SNPStats programs.
Results The genotype GG (p=0,02; OR=1,74, CI (1,12-2,72)) and allele G (p=0,03; OR=1,55, CI (1,06-2,28)) were found to be the genetic markers of increased JA risk. The earlier age debut of JA (0-6 years) was also was marked by the GG genotype (p=0,003). The GC or CC genotype were associated with the high JA activity (p=0,04). SNPStats program analysis indicated the association between the MIF*-173G>C SNP and JA in additive model (p=0,022, OR=0,63, 95%CI=0,42-0,94), dominant model (p=0,014, OR=0,57 95%CI=0,37-0,90), but not in recessive model (p=0,7, OR=0,79, 95%CI=0,23-2,74).
Conclusions Our data demonstrate the association of the polymorphic locus MIF*-173G>C with increased JA risk and clinical variants of the disease in patients from Bashkortostan, Russia.
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Disclosure of Interest None declared
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