ArticleThe Journal of clinical investigation2012
Anti-ganglioside antibody internalization attenuates motor nerve terminal injury in a mouse model of acute motor axonal neuropathy.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Unilateral facial palsy with hemiplegia and positive anti-GT1a antibody: a case report and literature review.Frontiers in immunology · 2026Review
- Guillain-Barré syndrome.Nature reviews. Disease primers · 2024Article
- Immune-Mediated Neuropathies: Pathophysiology and Management.International journal of molecular sciences · 2023Review
- The endogenous calpain inhibitor calpastatin attenuates axon degeneration in murine Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2023Article
- Septin-5 and -7-IgGs: Neurologic, Serologic, and Pathophysiologic Characteristics.Annals of neurology · 2022Article
- Guillain-Barré syndrome: expanding the concept of molecular mimicry.Trends in immunology · 2022Review
- Anti-disialoganglioside antibody internalization by neuroblastoma cells as a mechanism of immunotherapy resistance.Cancer immunology, immunotherapy : CII · 2022Article
- Autoimmune Peripheral Neuropathies and Contribution of Antiganglioside/Sulphatide Autoantibody Testing.Mediterranean journal of rheumatology · 2020Review
- Most of anti-glycolipid IgG-antibodies associated to neurological disorders occur without their IgM counterpart.Journal of biomedical science · 2019Article
- Cholesterol and the Safety Factor for Neuromuscular Transmission.International journal of molecular sciences · 2019Review
- Neurofilament light as an immune target for pathogenic antibodies.Immunology · 2017Article
- Modulation of IgG-FcRn interactions to overcome antibody-mediated inhibition of nerve regeneration.Acta neuropathologica · 2017Article
- Anti-ganglioside antibodies are removed from circulation in mice by neuronal endocytosis.Brain : a journal of neurology · 2016Article
- Circulating memory T follicular helper subsets, Tfh2 and Tfh17, participate in the pathogenesis of Guillain-Barré syndrome.Scientific reports · 2016Article
- Fluorescently-tagged anti-ganglioside antibody selectively identifies peripheral nerve in living animals.Scientific reports · 2015Article
- Effects of IgG anti-GM1 monoclonal antibodies on neuromuscular transmission and calcium channel binding in rat neuromuscular junctions.Experimental and therapeutic medicine · 2015Article
- Anti-Ganglioside Antibodies Induce Nodal and Axonal Injury via Fcγ Receptor-Mediated Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- New strategies in the management of Guillain-Barré syndrome.Clinical reviews in allergy & immunology · 2014Review
- The pre-synaptic motor nerve terminal as a site for antibody-mediated neurotoxicity in autoimmune neuropathies and synaptopathies.Journal of anatomy · 2014Review
- γ-Synuclein antibodies have neuroprotective potential on neuroretinal cells via proteins of the mitochondrial apoptosis pathway.PloS one · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the Guillain-Barré syndrome subform acute motor axonal neuropathy (AMAN), Campylobacter jejuni enteritis triggers the production of anti-ganglioside Abs (AGAbs), leading to immune-mediated injury of distal motor nerves. An important question has been whether injury to the presynaptic neuron at the neuromuscular junction is a major factor in AMAN. Although disease modeling in mice exposed to AGAbs indicates that complement-mediated necrosis occurs extensively in the presynaptic axons, evidence in humans is more limited, in comparison to the extensive injury seen at nodes of Ranvier. We considered that rapid AGAb uptake at the motor nerve terminal membrane might attenuate complement-mediated injury. We found that PC12 rat neuronal cells rapidly internalized AGAb, which were trafficked to recycling endosomes and lysosomes. Consequently, complement-mediated cytotoxicity was attenuated. Importantly, we observed the same AGAb endocytosis and protection from cytotoxicity in live mouse nerve terminals. AGAb uptake was attenuated following membrane cholesterol depletion in vitro and ex vivo, indicating that this process may be dependent upon cholesterol-enriched microdomains. In contrast, we observed minimal AGAb uptake at nodes of Ranvier, and this structure thus remained vulnerable to complement-mediated injury. These results indicate that differential endocytic processing of AGAbs by different neuronal and glial membranes might be an important modulator of site-specific injury in acute AGAb-mediated Guillain-Barré syndrome subforms and their chronic counterparts.
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