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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
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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