Association of CD1 and FcγR gene polymorphisms with Guillain–Barré syndrome susceptibility: a meta-analysis
- 95 Downloads
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.
KeywordsGuillain–Barré syndrome CD1 Fcgr Polymorphism Meta-analysis
We would like to express our sincere gratitude to all the participants for their efforts in this article.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
- 2.Cosi V, Versino M (2006) Guillain-Barre syndrome. Neurological Sciences:Official Journal of the Italian Neurol Sci 27(Suppl 1):S47–S51Google Scholar
- 4.Fukae J, Tsugawa J, Ouma S, Umezu T, Kusunoki S, Tsuboi Y (2016) Guillain-Barre and Miller Fisher syndromes in patients with anti-hepatitis E virus antibody: a hospital-based survey in Japan. Neurological sciences: official journal of the Italian Neurol Sci 37(11):1849–1851Google Scholar
- 5.Wang Y, Sun S, Zhu J, Cui L, Zhang H (2015) Biomarkers of Guillain-Barré syndrome: some recent progress, more still to be explored. Mediat Inflamm 2015:564098Google Scholar
- 15.Duits AJ, Bootsma H, Derksen RH, Spronk PE, Kater L, Kallenberg CG, Capel PJ, Westerdaal NA, Spierenburg GT, Gmeligmeyling FH (1995) Skewed distribution of IgG Fc receptor IIa (CD32) polymorphism is associated with renal disease in systemic lupus erythematosus patients. Arthritis Rheum 38(12):1832–1836CrossRefPubMedGoogle Scholar
- 25.Willison HJ, Jacobs BC, Van Doorn PA (2006) Guillain-Barré syndrome. Lancet 388(10045):1653–1666Google Scholar