Found 1 structure.
Displayed structure 1
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1. Compound ID: 8377
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a-Neup5Ac-(2-3)-+
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b-D-Galp-(1-3)-b-D-GalpNAc-(1-4)-b-D-Galp-(1-4)-b-D-Glcp-(1-1)-CER-(?--/ceramide/ |
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Structure type: oligomer
Aglycon: ceramide
Trivial name: GM1
Compound class: ganglioside
Contained glycoepitopes: IEDB_130648,IEDB_130678,IEDB_130679,IEDB_130683,IEDB_134627,IEDB_136044,IEDB_136794,IEDB_137339,IEDB_137472,IEDB_137473,IEDB_141794,IEDB_142487,IEDB_142488,IEDB_146100,IEDB_146664,IEDB_147450,IEDB_147451,IEDB_149174,IEDB_150933,IEDB_190606,IEDB_547903,IEDB_983931,SB_116,SB_13,SB_144,SB_164,SB_165,SB_166,SB_170,SB_171,SB_172,SB_187,SB_192,SB_195,SB_2,SB_23,SB_24,SB_25,SB_3,SB_37,SB_39,SB_4,SB_41,SB_5,SB_6,SB_68,SB_7,SB_71,SB_76,SB_8,SB_84,SB_88,SB_96
The structure is contained in the following publication(s):
- Article ID: 3646
Komagamine T, Yuki N "Ganglioside mimicry as a cause of Guillain-Barre syndrome" -
CNS and Neurological Disorders Drug Targets 5(4) (2006) 391-400
Guillain-Barre syndrome (GBS), characterized by acute progressive limb weakness and areflexia, is the prototype of postinfectious autoimmune diseases. Campylobacter jejuni is the most frequently identified agent of infection in GBS patients, often preceding acute motor axonal neuropathy (AMAN), a variant of GBS. Anti-GM1, anti-GM1b, anti-GD1a, and anti-GalNAc-GD1a IgG antibodies are associated with AMAN. Carbohydrate mimicry [Galβ1-3GalNAcβ1-4(NeuAcα2-3)Galβ1-] was seen between the lipo-oligosaccharide of C. jejuni isolated from an AMAN patient and human GM1 ganglioside. Sensitization with the lipo-oligosaccharide of C. jejuni induces AMAN in rabbits as does sensitization with GM1 ganglioside. Paralyzed rabbits have pathological changes in their peripheral nerves identical to changes seen in human GBS. C. jejuni infection may induce anti-ganglioside antibodies by molecular mimicry, eliciting AMAN. This is the first verification of the causative mechanism of molecular mimicry in an autoimmune disease. To express ganglioside mimics, C. jejuni requires specific gene combinations that function in sialic acid biosynthesis or transfer. The knockout mutants of these landmark genes of GBS show reduced reactivity with GBS patients' sera, and fail to induce an anti-ganglioside antibody response in mice. These genes are crucial for the induction of neuropathogenic cross-reactive antibodies. An approach for evaluating intravenous immune globulin, a treatment for GBS, based on our animal model of AMAN is also discussed in this review, and recent advances made in this field are described.
Campylobacter jejuni, ganglioside, Guillain-Barre syndrome, molecular mimicry, Autoimmune disease
NCBI PubMed ID: 16918391Journal NLM ID: 101269155Publisher: Bentham Science Publishers
Correspondence: yuki@dokkyomed.ac.jp
Institutions: Department of Neurology and Research Institute for Neuroimmunological Diseases, Dokkyo Medical University School of Medicine, Tochigi, Japan
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