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Association of CD1 and FcγR gene polymorphisms with Guillain–Barré syndrome susceptibility: a meta-analysis

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Abstract

CD1 and immunoglobulin G Fc receptor (FcγR) genes have been proposed to be involved in the pathogenesis of Guillain–Barré syndrome (GBS). However, results of different studies are conflicting. This meta-analysis aimed to systematically examine the association between CD1 and FcγR gene polymorphisms and GBS. A comprehensive literature search through PubMed, EmBase, ScienceDirect, and Cochrane Library was performed to identify all eligible studies. The strength of association was assessed by pooled odds ratios (ORs) and corresponding 95% confidence intervals (95% CI) in allelic, dominant, recessive, homozygous and heterozygous genetic models. Four case–control studies about polymorphisms of exon 2 in CD1A and CD1E genes and GBS risk and five studies (six cohorts) about FcγR gene polymorphisms and GBS risk were included in this meta-analysis. The association between exon 2 of CD1E gene polymorphism and GBS was marginally significant in Caucasians in allelic model (OR = 1.193, 95% CI = 1.001–1.423, P = 0.049). FcγRIIA gene polymorphism was significantly associated with GBS risk in Caucasians under allelic model (OR = 1.553, 95% CI = 1.018–2.368, P = 0.041) and dominant model (OR = 1.320, 95% CI = 1.027–1.697, P = 0.030). However, no significant association was found between polymorphisms in exon 2 of CD1A, FcγRIIIA and FcγRIIIB genes and GBS susceptibility. This meta-analysis suggested that FcγRIIA gene polymorphism may contribute to GBS risk in Caucasians and revealed a certain trend toward significance in the association of exon 2 of CD1E gene with GBS in Caucasians. Further studies with larger sample size are required to validate these results.

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We would like to express our sincere gratitude to all the participants for their efforts in this article.

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Correspondence to Jijun Teng.

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Zhang, L., Liu, L., Li, H. et al. Association of CD1 and FcγR gene polymorphisms with Guillain–Barré syndrome susceptibility: a meta-analysis. Neurol Sci 39, 2141–2149 (2018). https://doi.org/10.1007/s10072-018-3563-3

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  • DOI: https://doi.org/10.1007/s10072-018-3563-3

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