HLA-class II alleles in Guillain-Barré syndrome and Miller Fisher syndrome and their association with preceding Campylobacter jejuni infection

Rees, Jeremy; Vaughan, R. W.; Kondeatis, E; Hughes, Richard

doi:10.1016/0165-5728(95)00102-8

Cited by 95 publications

(58 citation statements)

References 13 publications

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“…When the seroreactivity status was evaluated in relationship to the HLA DRB1, DQB1, or DPB1 alleles or the RLD 55-57 /ED 70 -71 and RPD 55-57 DQ␤ epitopes among AIDP or AMAN patients, no significant correlation was established. No association was identified between seroreactivity status and DQ3 specificity in this Chinese population, as was suggested in studies on C. jejuni-associated GBS in European patients with AIDP (28). The lack of association in our population must be considered in light of the small population sampled in our study.…”

Section: Hla-drb1 and Hla-dpb1 Allele Distributioncontrasting

confidence: 42%

“…Rees et al (28) identified DQB1*03 as being associated with Campylobacter-positive GBS patients compared with seronegative patients; however, Yuki et al (56) did not confirm this in a different population. Our studies also did not find an allele association in either AIDP or AMAN with evidence of prior Campylobacter infection.…”

Section: Discussionmentioning

confidence: 74%

“…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%

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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: Hla-drb1 and Hla-dpb1 Allele Distributioncontrasting

confidence: 42%

Section: Discussionmentioning

confidence: 74%

Section: G Uillain-barré Syndrome (Gbs)mentioning

confidence: 99%

See 1 more Smart Citation

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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“…Hartung and Toyka (34) reported macrophage activation in GBS in which circulating activated T lymphocytes were found, as evidenced by augmented expression of histocompatibility antigens (HLA-DR), suggesting that there is an association between GBS and HLA alleles. In HLA typing for class II alleles, Rees et al (65) reported the association between HLA-DQB1*03 and preceding C. jejuni infection in GBS or Miller-Fisher syndrome. In AIDP patients, the DRB1*1301 allele showed a significant increase, but not in AMAN.…”

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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“…The presence of this epitope, therefore, is not alone responsible for causing GBS. Host genetic susceptibility to developing GBS following exposure to a strain with this virulence phenotype is likely to be a critical factor (30,35).…”

mentioning

confidence: 99%

Campylobacter jejunifrom Patients with Guillain-Barré Syndrome Preferentially Expresses a GD_1a-Like Epitope

Nachamkin

Liu

et al. 2002

Infect Immun

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GM 1 -and GD 1a -like ganglioside mimicry in Campylobacter jejuni lipooligosaccharide (LOS) is considered to be involved in the pathogenesis of Campylobacter-induced Guillain-Barré syndrome (GBS). Compared with gastroenteritis-related isolates, GBS-related C. jejuni isolates were strongly associated with the expression of GD 1a -like mimicry. The presence of a few genes involved in LOS ganglioside mimicry, cst-II, cgtA, and cgtB, was also associated with GBS-related strains. GD 1a -like epitope expression may be an important virulence phenotype associated with the risk of developing GBS following campylobacter infection.

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HLA-class II alleles in Guillain-Barré syndrome and Miller Fisher syndrome and their association with preceding Campylobacter jejuni infection

Cited by 95 publications

References 13 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

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

Campylobacter jejunifrom Patients with Guillain-Barré Syndrome Preferentially Expresses a GD_1a-Like Epitope

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HLA-class II alleles in Guillain-Barré syndrome and Miller Fisher syndrome and their association with preceding Campylobacter jejuni infection

Cited by 95 publications

References 13 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

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

Campylobacter jejunifrom Patients with Guillain-Barré Syndrome Preferentially Expresses a GD1a-Like Epitope

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Campylobacter jejunifrom Patients with Guillain-Barré Syndrome Preferentially Expresses a GD_1a-Like Epitope