SynthesisClinical rheumatology2018
Associations between interleukin-10 polymorphisms and susceptibility to rheumatoid arthritis: a meta-analysis and meta-regression.
Synthesis in Clinical rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Rheumatoid Arthritis: A Comprehensive Review of Etiology, Pathophysiology, and Innovative Therapeutic Advancements.Current pharmaceutical design · 2026Review
- Molecular analysis of TNFAIP3, PTPN22, IRF5, and IL-10 gene polymorphisms in palindromic rheumatism.Clinical rheumatology · 2025Article
- Associations of Gastrointestinal Tract Tumor Necrosis Factor Receptor-Associated Factor 6 Expression with Clinical Features and Prognosis of Eosinophilic Gastroenteritis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- The efficacy and safety of Huangqi Guizhi Wuwu decoction for rheumatoid arthritis: A protocol for systematic review and meta-analysis.Medicine · 2020Article
- Genetic Polymorphisms Associated with Rheumatoid Arthritis Development and Antirheumatic Therapy Response.International journal of molecular sciences · 2020Review
- Dose-dependent effects of oleuropein administration on regulatory T-cells in patients with rheumatoid arthritis: An in vitro approach.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
This study aimed to explore whether interleukin-10 polymorphisms are associated with susceptibility to rheumatoid arthritis (RA). Studies that have analyzed the associations of the interleukin-10-1082G>A, -592C>A, and -819C>T polymorphisms with RA were searched for in PubMed and EMBASE. Sensitivity and cumulative analyses were conducted to measure the robustness of our findings. Egger's linear regression and Begg's funnel plots were performed to analyze publication bias. The source of heterogeneity was analyzed by subgroup analysis and meta-regression. This meta-analysis involved 2661 RA patients and 3249 controls in 16 studies. There were significant associations with RA in the AG vs AA model (OR = 0.79, 95% CI = 0.67-0.93, P < 0.01) and the AG + GG vs AA model (OR = 0.80, 95% CI = 0.69-0.93, P < 0.01) for the interleukin-10-1082G>A polymorphism, in the TC vs TT model (OR = 0.61, 95% CI = 0.44-0.84, P < 0.01) and the CC vs TT model (OR = 0.64, 95% CI = 0.46-0.89, P < 0.01) for the interleukin-10-819C>T polymorphism, and in the AC vs AA model (OR = 0.73, 95% CI = 0.56-0.96, P = 0.03) and the AC + CC vs AA model (OR = 0.68, 95% CI = 0.47-0.98, P = 0.04) for the interleukin-10-592C>A polymorphism. Meta-regression revealed that the genotyping method was a major cause of heterogeneity in the AC vs AA model and the AC + CC vs AA model for the interleukin-10-592C>A polymorphism. This meta-analysis showed the interleukin-10-1082G>A, -592C>A, and -819C>T polymorphisms are correlated with the susceptibility to RA. Meta-regression indicated that the genotyping method is a major driver of heterogeneity in the relationship between the interleukin-10-592C>A polymorphism and RA.
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