Human Anti-Glycosphingolipids Antibodies in Guillain-Barré Syndrome

Robert K Yu, Seigo Usuki

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Guillain-Barré syndrome (GBS) is classified as a combination of several disorders and is characterized by an immune-mediated attack on the peripheral nervous system (PNS), particularly on the myelin sheath and axon of sensory and motor nerves, resulting in demyelination and/or axonal degeneration. Many of the previous clinical studies have suggested that GBS is most likely triggered by the appearance of enteritis and neuritis induced by microbial pathogens such as Campylobacter jejuni (. C. jejuni). There is evidence that interspecies transmission of C. jejuni-induced GBS can be transmitted from chickens to humans, but this possibility has not been epidemiologically demonstrated. The preceding infectious event is associated with increased antibody titers of glycosphingolipids (GSLs), especially certain acidic GSLs such as gangliosides and sulfoglycolipids, in patients with GBS. These anti-acidic GSL antibodies frequently express cross-reactivity between cell surface carbohydrate antigens of the infecting microbes and host cells. This cross-reactivity likely arises as the result of molecular mimicry between the carbohydrate epitopes and the GSLs of the PNS and bacterial (e.g., C. jejuni) lipo-oligosaccharides (LOS). Anti-ganglioside antibodies have been shown to involve about 60% of patients with GBS. Recently the presence of reacting antibodies with a mixed form of gangliosides (e.g., GD1a and GD1b) has been demonstrated. These antibodies have been overlooked and concealed in certain patients' sera that are "anti-ganglioside antibody negative." This unusual class of autoantibodies has been termed anti-ganglioside-complex (GSC) antibodies and is also implied in the pathogenesis of GBS and some of its variants. Pathogenically, these GBS-related antibodies have been shown to induce nerve injury, including demyelination and axonal degeneration, leading to serious loss of conduction velocity or conduction block. Recent studies also revealed that interruption of neurotransmission could occur as a result of interaction of anti-ganglioside antibodies with ion channels at the nodes of Ranvier. Accumulating ex  vivo electrophysiologic evidence suggests that ganglioside molecular mimicry may be responsible for muscle weakness, possibly via interference with ion channels as well as neuromuscular junctions.

Original languageEnglish (US)
Title of host publicationAutoantibodies
Subtitle of host publicationThird Edition
PublisherElsevier B.V.
Pages581-594
Number of pages14
ISBN (Print)9780444563781
DOIs
StatePublished - Dec 1 2013

Fingerprint

Glycosphingolipids
Gangliosides
Anti-Idiotypic Antibodies
Campylobacter jejuni
Acidic Glycosphingolipids
Antibodies
Molecular Mimicry
Peripheral Nervous System
Demyelinating Diseases
Ion Channels
Carbohydrates
Ranvier's Nodes
Neuritis
Enteritis
Neuromuscular Junction
Muscle Weakness
Surface Antigens
Myelin Sheath
Oligosaccharides
Synaptic Transmission

Keywords

  • Anti-carbohydrate antibody
  • Anti-ganglioside antibody
  • Autoimmunity
  • Bacterial infection
  • Carbohydrate molecular mimicry
  • Guillain-Barré syndrome
  • Peripheral neuropathy

ASJC Scopus subject areas

  • Immunology and Microbiology(all)

Cite this

Yu, R. K., & Usuki, S. (2013). Human Anti-Glycosphingolipids Antibodies in Guillain-Barré Syndrome. In Autoantibodies: Third Edition (pp. 581-594). Elsevier B.V.. https://doi.org/10.1016/B978-0-444-56378-1.00069-1

Human Anti-Glycosphingolipids Antibodies in Guillain-Barré Syndrome. / Yu, Robert K; Usuki, Seigo.

Autoantibodies: Third Edition. Elsevier B.V., 2013. p. 581-594.

Research output: Chapter in Book/Report/Conference proceedingChapter

Yu, Robert K ; Usuki, Seigo. / Human Anti-Glycosphingolipids Antibodies in Guillain-Barré Syndrome. Autoantibodies: Third Edition. Elsevier B.V., 2013. pp. 581-594
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