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Updated: Jul 16, 2026

Preparation of CD4+ T Cells for Analysis of GD3 and GD2 Ganglioside Membrane Expression by Microscopy
Published on: November 8, 2016
Ganglioside mimicry and peripheral nerve disease
1Department of Neurology and Research Institute for Neuroimmunological Diseases, Dokkyo Medical University School of Medicine, Kitakobayashi 880, Mibu, Shimotsuga, Tochigi 321-0293, Japan. yuki@dokkyomed.ac.jp
Abstract:
Four criteria must be satisfied to conclude that a given microorganism causes Guillain-Barré (GBS) or Fisher (FS) syndrome associated with anti-ganglioside antibodies: (1) an epidemiological association between the infecting microbe and GBS or FS; (2) isolation in the acute progressive phase of illness of that microorganism from GBS or FS patients with associated anti-ganglioside IgG antibodies; (3) identification of a microbial ganglioside mimic; and (4) a GBS or FS with associated anti-ganglioside antibodies model produced by sensitization with the microbe itself or its component, as well as with ganglioside. Campylobacter jejuni is a definitive causative microorganism of acute motor axonal neuropathy and may cause FS and related conditions. Haemophilus influenzae and Mycoplasma pneumoniae are possible causative microorganisms of acute motor axonal neuropathy or FS. Acute and chronic inflammatory demyelinating polyneuropathies may be produced by mechanisms other than ganglioside mimicry.
Insights
To confirm a microorganism causes Guillain-Barré (GBS) or Fisher syndrome (FS), four criteria are essential. Campylobacter jejuni is a definitive cause of certain neuropathies, while others are possible contributors.
Area of Science:
- Neuroimmunology
- Microbiology
- Neurology
Background:
- Guillain-Barré syndrome (GBS) and Fisher syndrome (FS) are often associated with anti-ganglioside antibodies.
- Establishing a causative link between microorganisms and these syndromes requires rigorous criteria.
Purpose of the Study:
- To outline the essential criteria for attributing GBS/FS to specific microorganisms.
- To identify microorganisms definitively or possibly linked to GBS/FS and anti-ganglioside antibodies.
Main Methods:
- Review and synthesis of established criteria for microbial causation of GBS/FS.
- Evaluation of evidence linking specific microbes (e.g., Campylobacter jejuni) to GBS/FS and anti-ganglioside antibodies.
- Consideration of ganglioside mimicry as a pathogenic mechanism.
Main Results:
- Four key criteria were defined: epidemiological association, microbial isolation, ganglioside mimicry, and experimental models.
- Campylobacter jejuni is identified as a definitive cause of acute motor axonal neuropathy and a potential cause of FS.
- Haemophilus influenzae and Mycoplasma pneumoniae are considered possible causes of these neuropathies.
Conclusions:
- Meeting the four defined criteria is crucial for establishing microbial causality in GBS/FS.
- Campylobacter jejuni has a strong association with specific GBS/FS subtypes.
- Other mechanisms may underlie acute and chronic inflammatory demyelinating polyneuropathies beyond ganglioside mimicry.
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