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Promoter polymorphism (−590, T/C) of interleukin 4 (IL4) gene is associated with rheumatoid arthritis: An updated meta-analysis

Rheumatoid arthritis (RA) is a chronic disease. It causes chronic inflammation of the joint. Recent studies suggested that interleukin 4 (IL4) contributes to susceptibility and severity of rheumatoid arthritis (RA). Especially, it was reported that promoter polymorphism (−590, T/C) of IL4 gene has b...

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Published in:Saudi journal of biological sciences 2017-02, Vol.24 (2), p.444-449
Main Authors: Park, Hyun Kyung, Kim, Su Kang, Kweon, Hae Yong, Lee, Kwan Gill, Arasu, Mariadhas Valan, Kim, Young Ock
Format: Article
Language:English
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Summary:Rheumatoid arthritis (RA) is a chronic disease. It causes chronic inflammation of the joint. Recent studies suggested that interleukin 4 (IL4) contributes to susceptibility and severity of rheumatoid arthritis (RA). Especially, it was reported that promoter polymorphism (−590, T/C) of IL4 gene has been associated with susceptibility of RA. The aim of present study was to investigate whether the promoter polymorphism (−590, T/C) of IL4 gene is associated with the susceptibility of RA using meta-analysis. And in order to perform meta-analysis, comprehensive meta analysis program was used. Genetic models (co-dominant, dominant, recessive, and allele) were used to determine odds ratios (ORs), 95% confidence intervals (CIs), and P values. Nine case-control studies with case and control design were included in this meta-analysis. Overall, meta-analysis revealed a strong association with susceptibility of RA [OR=1.303, 95% CI=1.093–1.554, P=0.003 in allele model (C vs. T); OR=1.247, 95% CI=1.054–1.474, P=0.010 in dominant model (CC vs. CT+TT); OR=2.148, 95% CI=1.263–3.651, P=0.005 in recessive model (CC+CT vs. TT)]. Our data demonstrated that promoter polymorphism (−590, T/C) of IL4 gene may be contributed to susceptibility of RA. However, more studies with a larger sample size are needed to provide more precise evidence.
ISSN:1319-562X
2213-7106
DOI:10.1016/j.sjbs.2016.01.013