Clinical features in Guillain–Barré syndrome with anti-Gal-C antibody

Samukawa, Makoto; Hamada, Yukihiro; Kuwahara, Motoi; Takada, Kazuo; Hirano, Minoru; Mitsui, Yosuke; Sonoo, Masahiro; Kusunoki, Susumu

doi:10.1016/j.jns.2013.11.016

Cited by 37 publications

(23 citation statements)

References 27 publications

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“…The cross-reactivity in these cases is likely induced by molecular mimicry between bacterial glycolipids and host myelin glycolipids, including GalC and gangliosides (Figure 2; figure references: [31]–[34]). Cross-reactive, anti-GalC antibodies have previously been detected in patients with Guillain-Barré syndrome (GBS) who suffered from a preceding M. pneumoniae infection [32], [35]–[38]. GBS is a typical postinfectious immune-mediated peripheral neuropathy [39].…”

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confidence: 99%

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Antibody Responses to Mycoplasma pneumoniae: Role in Pathogenesis and Diagnosis of Encephalitis?

et al. 2014

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confidence: 99%

“…In GBS, cross-reactive antibodies cause complement activation and formation of a membrane attack complex at the peripheral nerves, resulting in neuromuscular paralysis. Anti-GalC antibodies have been associated with demyelination in patients with GBS [35], [38]. Moreover, these anti-GalC antibodies cause neuropathy in rabbits that are immunized with GalC [40].…”

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confidence: 99%

Antibody Responses to Mycoplasma pneumoniae: Role in Pathogenesis and Diagnosis of Encephalitis?

et al. 2014

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“…It was the first animal model of neuropathy induced by individual glycolipid . Often, antibodies to Gal‐C localized at both peripheral nervous system (PNS) and central nervous system (CNS) myelin are detected in GBS or CNS diseases after M. pneumoniae infection . Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal‐C .…”

Section: Glycolipid Antibodies In Guillain‐barré Syndromementioning

confidence: 99%

“…Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal‐C . Based on electrophysiological studies, GBS cases with anti‐Gal‐C antibody are mostly classified as AIDP …”

Section: Glycolipid Antibodies In Guillain‐barré Syndromementioning

confidence: 99%

“…42 Often, antibodies to Gal-C localized at both peripheral nervous system (PNS) and central nervous system (CNS) myelin are detected in GBS or CNS diseases after M. pneumoniae infection. [43][44][45] Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal-C. 46,47 Based on electrophysiological studies, GBS cases with anti-Gal-C antibody are mostly classified as AIDP. 44,45 In GBS, the subclass of anti-glycolipid IgG antibody is predominantly IgG1 or IgG3, which activates the complement.…”

Section: Humoral Immunitymentioning

confidence: 99%

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Mechanism and spectrum of anti‐glycolipid antibody‐mediated chronic inflammatory demyelinating polyneuropathy

Kuwahara

Kusunoki

2018

Clinical & Exp Neuroim

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The pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP) is composed of cellular and humoral immunities. Macrophages might play a crucial role in cellular immunity. In addition, autoantibodies participate in the pathogenesis of CIDP. To date, various autoantibodies have been reported to affect peripheral nerve myelin. Although antibodies to glycolipids are frequently identified in Guillain‐Barré syndrome and closely related to the development of neuropathies, these are detected in only a small percentage of CIDP instances. Among glycolipids, sialosylneolactotetraosylceramide (LM1) is predominantly localized in human peripheral nerve myelin. LM1‐related antibodies (e.g. anti‐LM1, GM1/LM1 and GD1b/LM1 antibodies) are detected in some patients with CIDP and Guillain‐Barré syndrome. CIDP patients with those antibodies frequently present ataxia, but rarely have cranial nerve deficits; these features are associated with the localization of LM1, which is more abundant in the dorsal root than the cranial nerves. In immunoglobulin M paraproteinemic neuropathies, except for the anti‐myelin‐associated glycoprotein neuropathies, antibodies to glycolipids with disialosyl residues, such as GD1b and GQ1b, are also detected on occasion. Notably, this feature is clinically characterized by chronic ataxic neuropathy, ophthalmoplegia, immunoglobulin M paraprotein, cold agglutinins and disialosyl antibodies. Such clinical features are related to the localization of GD1b or GQ1b in human peripheral nerves. Overall, these correlations suggest a direct involvement of the antibodies in the pathogenesis of those aforementioned neuropathies.

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Mycoplasma pneumoniae triggering the Guillain‐Barré syndrome: A case‐control study

Sauteur

Huizinga

Tio‐Gillen

et al. 2016

Annals of Neurology

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Clinical features in Guillain–Barré syndrome with anti-Gal-C antibody

Cited by 37 publications

References 27 publications

Antibody Responses to Mycoplasma pneumoniae: Role in Pathogenesis and Diagnosis of Encephalitis?

Antibody Responses to Mycoplasma pneumoniae: Role in Pathogenesis and Diagnosis of Encephalitis?

Mechanism and spectrum of anti‐glycolipid antibody‐mediated chronic inflammatory demyelinating polyneuropathy

Mycoplasma pneumoniae triggering the Guillain‐Barré syndrome: A case‐control study

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