ArticleAnnals of clinical and translational neurology2019
Human leukocyte antigen-DQB1 polymorphisms and haplotype patterns in Guillain-Barré syndrome.
Article in Annals of clinical and translational neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
- Mammalian peripheral nerve specific autoimmunity: proposed mechanisms and redefinition of molecular mimicry.Frontiers in neurology · 2026Article
- Animal models of immune-mediated demyelinating polyneuropathies.Autoimmunity · 2024Review
- Association of mannose-binding lectin 2 gene polymorphisms with Guillain-Barré syndrome.Scientific reports · 2022Article
- Distribution of HLA Alleles and Genotypes in Patients with Chronic Inflammatory Demyelinating Polyneuropathy.Journal of molecular neuroscience : MN · 2022Article
- HLA-DQB1 mismatch increase risk of severe bleeding independently in recipients of allogeneic stem cell transplant.Annals of hematology · 2021Article
- Axonal variants of Guillain-Barré syndrome: an update.Journal of neurology · 2021Review
- A review of the role of genetic factors in Guillain-Barré syndrome.Journal of molecular neuroscience : MN · 2021Review
- NCAM protein and SARS-COV-2 surface proteins: In-silico hypothetical evidence for the immunopathogenesis of Guillain-Barré syndrome.Medical hypotheses · 2020Article
- Fc-gamma IIIa-V158F receptor polymorphism contributes to the severity of Guillain-Barré syndrome.Annals of clinical and translational neurology · 2020Article
- Severe Demyelinating Neuropathy in an Advanced Melanoma Patient Treated with Nivolumab plus Ipilimumab Combined Therapy.Case reports in oncologyArticle
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8 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveThe 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.
methodsHLA-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).
resultsNo 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.
interpretationThis 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.
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