Susceptibility to Guillain–Barré syndrome is associated to polymorphisms of CD1 genes

Caporale, Christina M.; Papola, F.; Fioroni, Maria Aurora; Aureli, Anna; Giovannini, Armando; Notturno, Francesca; Adorno, D.; Caporale, V.; Uncini, Antonino

doi:10.1016/j.jneuroim.2006.05.018

Cited by 79 publications

(63 citation statements)

References 38 publications

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“…CD1 genes are known to be located in human chromosome 1 (named CD1A, -B, -C, -D, and -E). Caporale et al (15) also reported that susceptibility to GBS is associated with polymorphisms of the CD1A and CD1E genes. Oligoclonal expansion of T cells bearing particular types of T-cell receptor V␤ and V␦ genes frequently occurs in GBS and Miller-Fisher syndrome (43).…”

Section: Genetic Predisposition Of Gbsmentioning

confidence: 97%

“…In addition, wla genes (wla cluster) that encode LOS biosynthesis (53) and the A(Ϫ670) GSNP in the promoter region of Fas and high levels of sFas (22) may be involved in the pathogenesis of GBS. Caporale et al (15) reported the association between GBS and CD1 molecules that are major histocompatibility complex-like glycoproteins specialized in capturing and presenting a variety of glycolipids to antigen-specific T cells. CD1 genes are known to be located in human chromosome 1 (named CD1A, -B, -C, -D, and -E).…”

Section: Genetic Predisposition Of Gbsmentioning

confidence: 99%

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Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases

2006

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Section: Genetic Predisposition Of Gbsmentioning

confidence: 97%

Section: Genetic Predisposition Of Gbsmentioning

confidence: 99%

Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases

2006

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“…10,11 However, research on candidate genes that could plausibly be involved in the pathogenesis of GBS has not been conclusive. For instance, increased susceptibility to GBS in association with polymorphisms in CD1, low-affinity immunoglobulin gamma Fc region receptors II-a and II-b (FcRII-a and FcRII-b), [12][13][14] and interleukin-10 genes still awaits validation. [15][16][17] In parallel, a large body of research has investigated the possible association between GBS and infections.…”

Section: Introductionmentioning

confidence: 99%

The Guillain–Barrè peptide signatures: from Zika virus to Campylobacter, and beyond

Lucchese¹,

Kanduc²

2017

VAAT

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Scientific attention has focused recently on the link between Guillain-Barrè syndrome (GBS) and Zika virus (ZIKV). Two related questions emerged: 1) what triggered the violent 2014 outbreak of a virus, which, first identified in 1947, had caused only a limited number of documented cases of human infection until 2007 and 2) which molecular mechanism(s) relate ZIKV active infection to GBS, an autoimmune inflammatory polyradiculoneuropathy. Capitalizing on the increased interest on ZIKV and hypothesizing the involvement of autoimmune mechanisms, we searched for minimal epitopic determinants shared between ZIKV and other GBS-related pathogens -namely, Epstein-Barr virus, human cytomegalovirus, influenza virus, Campylobacter jejuni, and Mycoplasma pneumoniae, among others -and human proteins that, when altered, have been associated with myelin disorders and axonopathies. We report a considerable peptide matching that links GBS-related pathogens to human proteins related to myelin disorders and axonopathies. Crucially, the shared pentapeptides repeatedly occur throughout numerous epitopes validated as immunopositive by a conspicuous scientific literature. The data support a scenario where multiple different infections over time and resulting multiple cross-reactions may contribute to the pathogenesis of GBS. In practice, previous infection(s) might create immunologic memory able to trigger uncontrolled hyperimmunogenicity during a successive pathogen exposure. ZIKV pandemic appears to be an exemplar model for a proofof-concept of such multiple cross-reactivity mechanism.

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“…These alleles have been investigated in GBS, but with conflicting results. An Italian study found that subjects with CD1E*01/01 genotype are 2.5 times more likely to develop GBS whereas subjects with CD1A*01/02 or CD1E*01/02 have a reduced relative risk (Caporale, Papola et al 2006). This was, however, not confirmed in a larger Dutch study using similar techniques (Kuijf, Geleijns et al 2008), and a subsequent metaanalysis found no difference .…”

Section: Cd1mentioning

confidence: 94%

“…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: 99%

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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Susceptibility to Guillain–Barré syndrome is associated to polymorphisms of CD1 genes

Cited by 79 publications

References 38 publications

Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases

Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases

The Guillain–Barrè peptide signatures: from Zika virus to Campylobacter, and beyond

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

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Susceptibility to Guillain–Barré syndrome is associated to polymorphisms of CD1 genes

Cited by 79 publications

References 38 publications

Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases

Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases

The Guillain&ndash;Barr&egrave; peptide signatures: from Zika virus to Campylobacter, and beyond

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

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The Guillain–Barrè peptide signatures: from Zika virus to Campylobacter, and beyond