However, further studies are necessary to investigate the CD1A*01/CD1E*01 haplotype distribution and its potential causative role in the axonal form of GBS.
Furthermore, subjects with CD1A*01/02 had a 2.9 times lower risk of developing GBS, and those with CD1A*02/02 had a 2.5 times higher risk to developing GBS than the controls, while there was no association between polymorphisms of CD1E genes and the susceptibilities to GBS.
SNPs in CD1A and CD1E were not associated with GBS susceptibility, specific clinical subgroups, anti-ganglioside antibodies, antecedent infections and prognosis.
Although a correlation between CD1E*01/01 genotype and recent C. jejuni infection or presence of antiganglioside antibodies was not found the overall findings indicate that susceptibility to develop GBS is associated with polymorphisms of CD1E and CD1A genes.