Genetic predisposition of IL-10 promoter polymorphisms with risk of multiple sclerosis: A meta-analysis

- Interleukin-10 inhibits the synthesis of several cytokines including IL-2, IL-3, IFN-γ, and TNF-α.
- Polymorphisms in IL-10 modulate its mRNA expression that plays a vital role in neuroinflammation.
- The genetic predisposition of IL-10 promoter polymorphisms and risk of multiple sclerosis remains contradictory.
- rs1801896, rs1800872 and rs1800871 polymorphisms with MS susceptibility was examined.
- rs1801896, rs1800872, rs1800871 polymorphisms were not associated with MS in Asian and Caucasian populations.

Interleukin-10 (IL-10) is a anti-inflammatory cytokine, which controls inflammation by inhibiting the synthesis of several cytokines produced by Th1 cells and macrophages. The association between Interleukin-10 promoter polymorphisms with the risk of multiple sclerosis (MS) remains inconclusive. In this study, a meta-analysis has been performed to assess the relationship between IL-10 gene polymorphisms rs1800896, rs1800871 and rs1800872 with the risk of MS. Nine case-control studies were selected involving 2755 participants. The association between the polymorphisms and MS was examined by the pooled odds ratios (ORs) with 95% confidence intervals (CIs) in allelic, homozygote, heterozygote, dominant and recessive genetic models. Of analyzed genetic models, the pooled ORs and CIs of each SNPs calculated based on random (I2 > 50) or fixed effects (I2 < 50) methods, which showed no significant association (p-value > 0.05) of genetic predisposition with MS susceptibility across Asian and Caucasian populations. In addition, assessment based on funnel plot and Egger's linear regression test suggests no publication bias in all analyzed genetic models. Overall, our results demonstrated that rs1800896, rs1800871 and rs1800872 polymorphisms may not be the risk factor for the development of MS in both the populations.