Human leukocyte antigen-DQB1 polymorphisms and haplotype patterns in Guillain-Barré syndrome

The etiology of Guillain-Barré syndrome (GBS) remains enigmatic, although genetic and environmental factors are speculated to be associated with this autoimmune condition. We investigated whether polymorphisms and the haplotype structures of the human leukocyte antigen (HLA)-DQB1 gene relate to the autoimmune response to infection and affect the development of GBS.

HLA-DQB1 polymorphic alleles (*0201, *030x, *0401, *050x, *060x) were determined for 151 Bangladeshi patients with GBS and 151 ethnically matched healthy controls using sequence-specific polymerase chain reaction. Pairwise linkage disequilibrium (LD) and haplotype patterns were analyzed based on D ́statistics and the genotype package in R statistics, respectively. Association studies were conducted using Fisher's exact test and logistic regression analysis. The Bonferroni method was applied to correct for multiple comparisons, whereby the P-value was multiplied with the number of comparisons and denoted as Pc (Pc, P corrected).

No associations were observed between HLA-DQB1 alleles and susceptibility to disease in the comparison between GBS patients and healthy subjects. Haplotype 9 (DQB1*0303-*0601) tended to be less frequent among patients with GBS than healthy controls (P = 0.006, OR = 0.49, 95% CI = 0.30-0.82; Pc = 0.06). Haplotype 5 (DQB1*0501-*0602) and the DQB1*0201 alleles were more frequent in the Campylobacter jejuni-triggered axonal variant of GBS (P = 0.024, OR = 4.06, 95% CI = 1.25-13.18; Pc = 0.24) and demyelinating subtype (P = 0.027, OR = 2.68, 95% CI = 1.17-6.17; Pc = 0.35), though these associations were not significant after Bonferroni correction.

This study indicates that HLA-DQB1 polymorphisms are not associated with susceptibility to GBS. In addition, these genetic markers did not influence the clinical features or serological subgroup in patients with C. jejuni-triggered axonal variant of GBS.