HLA antigens in the Guillain-Barré syndrome

Winer, John; Briggs, David; Welsh, K; Hughes, Richard

doi:10.1016/0165-5728(88)90130-0

Cited by 40 publications

(18 citation statements)

References 12 publications

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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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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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“…The best evidence is of TNFα polymorphisms, which have been described in several studies ). For some of these genes, namely HLA and CD1, there are conflicting results between studies (Gorodezky, Varela et al 1983, Winer, Briggs et al 1988, Magira, Papaioakim et al 2003, Caporale, Papola et al 2006, Kuijf, Geleijns et al 2008). Other genes have been studied, but no association has been found.…”

Section: Relevant Negativesmentioning

confidence: 98%

“…Early studies using serological methods generally found no HLA association (Latovitzki, Suciu-Foca et al 1979, Kaslow, Sullivan-Bolyai et al 1984, Hafez, Nagaty et al 1985, although one study in Mexico found that GBS was associated with carriage of HLA-DR3 (Gorodezky, Varela et al 1983). The majority of these studies have not found any associations between GBS and carriage of class I or class II HLA molecules (Winer, Briggs et al 1988, Piradov, Dolbin et al 1995. However, when GBS patients have been grouped according to whether they have AIDP or axonal neuropathy, it has been found that certain DQB1 molecules are associated with AIDP but not axonal neuropathy (Magira, Papaioakim et al 2003).…”

Section: Hla Genesmentioning

confidence: 99%

“…Polymorphisms in HLA and CD1 have both been found in GBS cohorts, but these findings could not be confirmed in a larger sample (Gorodezky, Varela et al 1983, Winer, Briggs et al 1988. A range of other genes, including IL-10, TNF-α, MMP9, Fc receptors and LPS receptors have been studied in single, un-replicated studies (see Chapter 2 and 6).…”

Section: A Genetic Basis Of Gbs Pathogenesis?mentioning

confidence: 99%

“…Indeed, for many autoimmune diseases, the HLA locus hosts the strongest and most consistent susceptibility alleles (Rai and Wakeland 2011). In GBS, HLA has been extensively studied, with some conflicting results, but no clear and reproducible link has been established so far (Gorodezky, Varela et al 1983, Winer, Briggs et al 1988, Magira, Papaioakim et al 2003, Geleijns, Schreuder et al 2005. Whilst not conclusive, this argues against a dominant role of the adaptive immune system in GBS pathogenesis.…”

Section: Relevant Negativesmentioning

confidence: 99%

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Immunogenetic studies of Guillain - Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Blum¹

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Guillain-Barre syndrome (GBS) is an acute inflammatory neuropathy that is frequently triggered by an infectious illness. It is thought to be autoimmune in origin, but differs from other autoimmune diseases in being of male predominance and not showing a HLA-association.Chronic inflammatory demyelinating polyradiculoneuropathy is a chronic inflammatory neuropathy, which shares some pathological features with GBS.We investigated the clinical features of GBS in an Australian cohort of subjects by performing a retrospective chart review. We obtained subjects from several public hospitals and private neurologists in Queensland and New South Wales.We found 335 patients, for 228 of whom electrophysiological data was available. Of these acute inflammatory demyelinating polyradiculoneuropathy (AIDP) with 168 cases was the most common form, whilst axonal and focal forms were rarer. We identified upper respiratory tract infections, occurring predominantly in winter months, as the most frequently named triggering factor for GBS.The illness severity in our cohort was similar to that in earlier Australian studies.Also, we identified a cohort of 78 subjects fulfilling diagnostic criteria for CIDP from similar sources.We investigated a possible underlying genetic susceptibility to develop GBS or CIDP by contacting members of this cohort and collecting their DNA. We embarked on both a candidate gene approach to investigate the killer immunoglobulin-like receptors (KIRs) and their HLA ligands, as well as performing a genome-wide association study (GWAS) of the subjects with GBS as a hypothesis-free method.For the KIR/HLA system, whilst no significant differences were detected in the frequency of KIR genes, HLA-C2 and HLA-B Bw4-T were more frequent in subjects with GBS than controls (p<0.001). The inhibitory pairs of KIR-2DL2/HLA-C2 and KIR-3DL1/HLA-B Bw4-T were more frequent in GBS than controls (p<0.005). Whilst there were some differences between CIDP subjects and controls, interestingly, there were no difference between subjects with GBS and CIDP.This could point to similarities of pathogenesis between these two inflammatory neuropathies.A GWAS was performed on a largely identical cohort of 190 subjects with GBS. Whilst this cohort is relatively small for a modern GWAS and no genome-wide significant results were expected, we were able to identify a number of regions of interest based on clusters of SNPs in linkage disequilibrium of increased significance. These included rs10519519 on Chromosome 2, which is associated with MYT1L, a transcription factor in neuronal development; rs7663689 on Chromosome 4, which is in the promotor region of IL15; rs11151180 on Chromosome 18 which is in a gene-free region; rs17095496 on Chromosome 14, which amongst other genes is associated with DACT1, which encodes a regulator of cell division involved in the NF-κB pathway; and rs2302524 on chromosome 19, associated among other genes with NFKBIB, which encodes an inhibitor of the NF-κB pathway. Relative negatives included the HLA region, a...

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Immunopathogenesis and treatment of the guillain‐barré syndrome—part I

et al. 1995

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The etiology of the Guillain-Barré syndrome (GBS) still remains elusive. Recent years have witnessed important advances in the delineation of the mechanisms that may operate to produce nerve damage. Evidence gathered from cell biology, immunology, and immunopathology studies in patients with GBS and animals with experimental autoimmune neuritis (EAN) indicate that GBS results from aberrant immune responses against components of peripheral nerve. Autoreactive T lymphocytes specific for the myelin antigens P0 and P2 and circulating antibodies to these antigens and various glycoproteins and glycolipids have been identified but their pathogenic role remains unclear. The multiplicity of these factors and the involvement of several antigen nonspecific proinflammatory mechanisms suggest that a complex interaction of immune pathways results in nerve damage. Data on disturbed humoral immunity with particular emphasis on glycolipid antibodies and on activation of autoreactive T lymphocytes and macrophages will be reviewed. Possible mechanisms underlying initiation of peripheral nerve-directed immune responses will be discussed with particular emphasis on the recently highlighted association with Campylobacter jejuni infection.

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HLA antigens in the Guillain-Barré syndrome

Cited by 40 publications

References 12 publications

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

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

Immunogenetic studies of Guillain - Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Immunopathogenesis and treatment of the guillain‐barré syndrome—part I

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