Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Meta-Analysis
. 2017 Apr 26;7(1):1207.
doi: 10.1038/s41598-017-01345-8.

Variants in the IL7RA gene confer susceptibility to multiple sclerosis in Caucasians: evidence based on 9734 cases and 10436 controls

Hong Liu  1   2 , Jian Huang  3 , Mengmeng Dou  1   2 , Yong Liu  2   4 , Biying Xiao  5 , Xu Liu  6 , Zunnan Huang  7   8   9
Affiliations
Meta-Analysis

Variants in the IL7RA gene confer susceptibility to multiple sclerosis in Caucasians: evidence based on 9734 cases and 10436 controls

Hong Liu et al. Sci Rep. .

Abstract

Recently, numerous genome wide association studies (GWAS) and other case-control association studies examining the relationship between interleukin-7 receptor α chain (IL7RA) gene rs3194051, rs987107, rs11567686, and rs11567685 variants and multiple sclerosis (MS) risk have been conducted, but the conclusions have been inconsistent. The main objective of this meta-analysis was to more precisely explore the association of these four IL7RA variants with MS development. Twenty-seven eligible studies involving 9734 cases and 10436 controls were included in the present meta-analysis. Power calculation, publication bias, sensitivity analysis and cumulative meta-analysis were performed to derive a reliable conclusion. Our study indicated three IL7RA loci were significantly associated with increasing MS risk (rs3194051: recessive model: OR = 1.22, 95% CI 1.08-1.38; rs987107: recessive model: OR = 1.44, 95% CI 1.22-1.69; and rs11567686: dominant model: OR = 1.18, 95% CI 1.01-1.37). Additionally, IL7RA rs11567685 variants might not be related to MS development. In all, IL7RA locus polymorphisms could play an important role in the predisposition to MS, which could contribute to a better understanding the pathogenesis of multiple sclerosis.

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Flow diagram of the process used to select eligible studies.
Figure 2
Figure 2
Forest plots of IL7RA polymorphisms and the risk of multiple sclerosis: (A): rs3194051 polymorphism under the recessive model (GG vs. GA + AA); (B): rs987107 polymorphism under the recessive model (TT vs. TC + CC); (C): rs11567686 polymorphism under the dominant model (GG + GA vs. AA); (D): rs11567685 polymorphism under the allelic model (C vs. T).
Figure 3
Figure 3
Forest plot of cumulative meta-analysis by sample size about the association between the rs987107 polymorphism and MS risk under the recessive model.
Figure 4
Figure 4
Funnel plot for the recessive model to analyze publication bias of the association of the rs987107 polymorphism with MS risk.
See this image and copyright information in PMC

References

    1. Compston A, Coles A. Multiple sclerosis. Lancet. 2008;372:1502–1517. doi: 10.1016/S0140-6736(08)61620-7. - DOI - PubMed
    1. Rosati G. The prevalence of multiple sclerosis in the world: an update. Neurol Sci. 2001;22:117–139. doi: 10.1007/s100720170011. - DOI - PubMed
    1. Tullman MJ. Overview of the epidemiology, diagnosis, and disease progression associated with multiple sclerosis. Am J Manag Care. 2013;19:S15–20. - PubMed
    1. Hauser SL, Oksenberg JR. The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. Neuron. 2006;52:61–76. doi: 10.1016/j.neuron.2006.09.011. - DOI - PubMed
    1. Owens GM, Olvey EL, Skrepnek GH, Pill MW. Perspectives for managed care organizations on the burden of multiple sclerosis and the cost-benefits of disease-modifying therapies. J Manage Care Pharm. 2013;19:S41–S53. - PMC - PubMed

Publication types

MeSH terms

Substances