HLA antigens in Guillain‐Barré Syndrome

Kaslow, Richard A.; Sullivan-Bólyai, John Z.; Hafkin, Barry; Schonberger, L. B.; Kraus, L.; Moore, Michael J.; Yunis, Edmond J.; Williams, Roger M.

doi:10.1212/wnl.34.2.240

Cited by 36 publications

(9 citation statements)

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“…One study assessed the possible association of HLA types among cases of GBS identified during the 1976 vaccine surveillance effort [31]. Ninety-two cases of GBS (38 vaccinated, 54 unvaccinated) that were identified during the national surveillance effort were recruited, and each case was asked to recruit as a control participant either a spouse or a neighbor/associate of the same sex matched for age, race and history of A/NJ/76(H1N1) influenza immunization.…”

Section: Influenza Vaccine and Guillain-barré Syndrome: Biological Evmentioning

confidence: 99%

Guillain-Barré Syndrome Following Influenza Vaccination: Causal or Coincidental?

Sejvar

Pfeifer

Schonberger

2011

Curr Infect Dis Rep

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In 1976, the emergence of a new swine-origin influenza virus prompted concerns about an impending influenza pandemic. Although the outbreak never materialized, the epidemiological link between Guillain-Barre syndrome, a potentially severe peripheral nerve disorder, and the influenza vaccines developed against this virus caught public health officials, clinicians, and the public by surprise. Subsequently, a great deal of scrutiny has been placed on the possible risk of other formulations of influenza vaccine causing this adverse event. Several epidemiologic and biological assessments have been performed in subsequent years to assess this risk, yet considerable uncertainty remains among health care providers about the possible association. The development and rapid implementation of vaccines against the pandemic 2009 A(H1N1) influenza virus once again highlighted this issue. This article reviews the evidence for and against the association of the 1976 influenza vaccines and subsequent seasonal influenza vaccines with the development of Guillain-Barré syndrome.

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Section: Influenza Vaccine and Guillain-barré Syndrome: Biological Evmentioning

confidence: 99%

Guillain-Barré Syndrome Following Influenza Vaccination: Causal or Coincidental?

Sejvar

Pfeifer

Schonberger

2011

Curr Infect Dis Rep

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“…There have been several studies of HLA associations with GBS, with a variety of associations identified; however, patients have not been characterized according to disease subtype, and this may explain the lack of consistent findings (23)(24)(25)(26)(27)(28). We have had the unique opportunity to study GBS in a population of individuals from northern China who developed both AIDP and AMAN forms of GBS (6,9,29).…”

Section: G Uillain-barré Syndrome (Gbs)mentioning

confidence: 99%

Differential Distribution of HLA-DQβ/DRβ Epitopes in the Two Forms of Guillain-Barré Syndrome, Acute Motor Axonal Neuropathy and Acute Inflammatory Demyelinating Polyneuropathy (AIDP): Identification of DQβ Epitopes Associated with Susceptibility to and Protection from AIDP

Magira

Papaioakim²,

Nachamkin³

et al. 2003

The Journal of Immunology

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Guillain-Barré syndrome (GBS), an acute, immune-mediated paralytic disorder affecting the peripheral nervous system, is the most common cause of acute flaccid paralysis in the postpolio era. GBS is classified into several subtypes based on clinical and pathologic criteria, with acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) being the most common forms observed. To better understand the pathogenesis of GBS and host susceptibility to developing the disease, the distribution of HLA class II Ags along with the seroreactivity to Campylobacter jejuni were investigated in a population of GBS patients from northern China. Using DNA-based typing methods, 47 patients with AMAN, 25 patients with AIDP, and 97 healthy controls were studied for the distribution of class II alleles. We found that the DQβ RLD55–57/ED70–71 and DRβ E9V11H13 epitopes were associated with susceptibility to AIDP (p = 0.009 and p = 0.004, respectively), and the DQβ RPD55–57 epitope was associated with protection (p = 0.05) from AIDP. These DQβ/DRβ positional residues are a part of pockets 4 (DQβ 70, 71, DRβ13), 6 (DRβ11), and 9 (DQβ 56, 57, DRβ9); have been demonstrated to be important in peptide binding and T cell recognition; and are associated with other diseases that have a pathoimmunological basis. Class II HLA associations were not identified with AMAN, suggesting a different immunological mechanism of disease induction in the two forms of GBS. These findings provide immunogenetic evidence for differentiating the two disease entities (AMAN and AIDP) and focuses our attention on particular DRβ/DQβ residues that may be instrumental in understanding the pathophysiology of AIDP.

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“…Genes that have been looked at include HLA-A (with a single study showing slight reduction in HLA11 in GBS), HLA-B (with increased isoleucine carriage at position 80 of Bw4 alleles), HLA-C (with increased carriage of alleles with lysine at position 80), HLA-DPB1, HLA-DQA1, HLA-DQB1 (with increased HLA-DQB1*03 in patients with Clostridium jejuni infection in a single study, DQ epitopes associated with AIDP but not AMAN in another study and increased DQ*06 in another study; these studies were from disparate populations) and HLA-DRB1 (with 4 out of 13 studies showing some association: increased DR3, increased DRB1*13, increased DRB1 epitopes, HLA-DRB1*14 and DRB1*13 with haplotypes DRB1*14/DQB1*05 and DRB1*13/DQB1*03 conferring susceptibility, and haplotypes DRB1*07/DQB1*02 and DRB1*03/DQB1*02 conferring protection against GBS, and DRB1*0701 increased in GBS patients with preceding infection) [11,61,10,111,90,33]. …”

Section: Introductionmentioning

confidence: 99%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

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HLA antigens in Guillain‐Barré Syndrome

Cited by 36 publications

References 0 publications

Guillain-Barré Syndrome Following Influenza Vaccination: Causal or Coincidental?

Guillain-Barré Syndrome Following Influenza Vaccination: Causal or Coincidental?

Differential Distribution of HLA-DQβ/DRβ Epitopes in the Two Forms of Guillain-Barré Syndrome, Acute Motor Axonal Neuropathy and Acute Inflammatory Demyelinating Polyneuropathy (AIDP): Identification of DQβ Epitopes Associated with Susceptibility to and Protection from AIDP

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

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