A5015541361- Peripheral Neuropathies and Disorders
- Hereditary Neurological Disorders
- Nerve injury and regeneration
- Autoimmune Neurological Disorders and Treatments
- Myasthenia Gravis and Thymoma
- Monoclonal and Polyclonal Antibodies Research
- Peripheral Nerve Disorders
- Glycosylation and Glycoproteins Research
- Botulinum Toxin and Related Neurological Disorders
- Complement system in diseases
- Pain Mechanisms and Treatments
- Long-Term Effects of COVID-19
- Pharmacological Effects of Natural Compounds
- Infectious Diseases and Tuberculosis
- Clostridium difficile and Clostridium perfringens research
- Galectins and Cancer Biology
- Salmonella and Campylobacter epidemiology
- SARS-CoV-2 and COVID-19 Research
- Facial Nerve Paralysis Treatment and Research
- Neurogenetic and Muscular Disorders Research
- Multiple Sclerosis Research Studies
- Viral Infections and Immunology Research
- Parkinson's Disease and Spinal Disorders
- Toxin Mechanisms and Immunotoxins
- Autoimmune Bullous Skin Diseases
Chinese Academy of Sciences
2025
Tenri Hospital
2024
National University of Singapore
2010-2017
Dokkyo Medical University
2005-2017
National University Hospital
2012-2017
Centre de Recherche en Neurobiologie - Neurophysiologie de Marseille
2016
Centre National de la Recherche Scientifique
2016
Aix-Marseille Université
2016
The University of Sydney
2015-2016
Showa University Fujigaoka Hospital
2016
There is a strong association between Guillain-Barré syndrome (GBS) and Penner's serotype 19 (PEN 19) of Campylobacter jejuni. Sera from patients with GBS after C. jejuni infection have autoantibodies to GM1 ganglioside in the acute phase illness. Our previous work has suggested that results an immune response cross-reactive antigen lipopolysaccharide (LPS) Gram-negative bacterium membrane components peripheral nerves. To clarify pathogenesis GBS, we investigated whether GM1-oligosaccharide...
Molecular mimicry between microbial and self-components is postulated as the mechanism that accounts for antigen tissue specificity of immune responses in postinfectious autoimmune diseases. Little direct evidence exists, research this area has focused principally on T cell-mediated, antipeptide responses, rather than humoral to carbohydrate structures. Guillain–Barré syndrome, most frequent cause acute neuromuscular paralysis, occurs 1–2 wk after various infections, particular,...
We report 2 patients with Guillain-Barré syndrome (GBS) following <i>Campylobacter jejuni</i> enteritis. Electrophysiologic studies indicated that the predominant process was axonal degeneration of motor nerves, and clinical recovery poor. Serum testing by thin-layer chromatography enzyme-linked immunosorbent assay revealed sera from both contained high titers IgG antibody against GM<sub>1</sub> ganglioside. These cases may represent a subgroup GBS as acute polyneuropathy <i>C enteritis...
The authors reviewed the clinical features and outcome of Miller Fisher syndrome (MFS) for 50 consecutive patients with MFS including 28 who received no immunotherapy. Besides characteristic triad (ophthalmoplegia, ataxia, areflexia), pupillary abnormalities, blepharoptosis, facial palsy are frequent in MFS, whereas sensory loss is unusual despite presence profound ataxia. Patients usually had good recovery residual deficits.
Voltage-gated Na + (Na v ) channels are highly concentrated at nodes of Ranvier in myelinated axons and facilitate rapid action potential conduction. Autoantibodies to gangliosides such as GM1 have been proposed disrupt nodal Nav lead Guillain-Barré syndrome, an autoimmune neuropathy characterized by acute limb weakness. To test this hypothesis, we examined the molecular organization a disease model caused immunization with gangliosides. At phase progressing weakness, channel clusters were...
We report the clinical and serologic features of Japanese patients with chronic inflammatory demyelinating polyneuropathy (CIDP) displaying anti-neurofascin-155 (NF155) immunoglobulin G4 (IgG4) antibodies.
We asked whether autoantibodies against neurofascin (NF)186 or NF155, both localized at the nodes of Ranvier, are present in serum patients with inflammatory neuropathy, and NF-specific monoclonal antibodies pathogenic vivo.We cloned human NF155 NF186, developed an ELISA cell-based assay to screen for NF a total 434 donors including 294 Guillain-Barré syndrome variants acute demyelinating polyneuropathy (AIDP), motor axonal chronic (CIDP). characterized reactive samples by isotyping, tissue...
Chronic inflammatory demyelination polyneuropathy is a heterogeneous and treatable immune-mediated disorder that lacks biomarkers to support diagnosis. Recent evidence indicates paranodal proteins (contactin 1, contactin-associated protein neurofascin-155) are the targets of autoantibodies in subsets patients showing distinct clinical presentations. Here, we identified neurofascin-186 neurofascin-140 as main five presenting IgG reactivity against nodes Ranvier. Four displayed predominantly...
A Spanish group recently reported that four patients with chronic inflammatory demyelinating polyneuropathy carrying IgG4 autoantibodies against contactin 1 showed aggressive symptom onset and poor response to intravenous immunoglobulin. We aimed describe the clinical serological features of Japanese displaying anti-contactin antibodies. Thirteen 533 (2.4%) had whereas neither from disease or normal control subjects did (P = 0.02). Three 13 (23%) subacute onset, but all presented sensory...
To clarify the relations of axonal form Guillain-Barré syndrome (GBS) to anti-ganglioside antibodies and Campylobacter jejuni infection, 86 consecutive Japanese GBS patients were studied. Electrodiagnostic criteria showed acute inflammatory demyelinating polyneuropathy in 36% motor neuropathy (AMAN) 38%. Frequent IgG class against GM1 (40%), GD1a (30%), GalNAc-GD1a (17%), GD1b (21%). Identified infections C. (23%), cytomegalovirus (10%), Mycoplasma pneumoniae (6%), Epstein-Barr virus (3%)....
Some humans develop the axonal form of Guillain-Barré syndrome after receiving bovine brain ganglioside. On sensitization with ganglioside mixture, all a group rabbits injected developed high anti-GM1 IgG antibody titers, flaccid limb weakness acute onset, and monophasic illness course. Pathological findings for peripheral nerves showed predominant Wallerian-like degeneration, neither lymphocytic infiltration nor demyelination. was deposited on axons anterior roots, GM1 proved to be present...
Abstract To investigate the pathophysiological role of anti‐GM1 antibody in Gullain‐Barre syndrome (GBS), we reviewed sequential nerve conduction studies 345 nerves 34 GBS patients. Statistically significant correlation between IgG antibodies and electrodiagnoses was found. Sixteen anti‐GM1‐positive patients were classified as having acute motor sensory axonal neuropathy (AMAN or AMSAN) (12 patients), inflammatory demyelinating polyneuropathy (AIDP) (3 patientsrpar;, undetermined (1 patient)...
<b>Objective: </b> To assess the production mechanism of anti-GQ1b autoantibody in Fisher syndrome (FS). <b>Methods: The authors conducted a prospective case-control serologic study five antecedent infections (<i>Campylobacter jejuni</i>, cytomegalovirus, Epstein–Barr virus, <i>Mycoplasma pneumoniae</i>, and <i>Haemophilus influenzae</i>) 73 patients with FS sex- age-matched hospital controls (HCs). Serologic evidence <i>C. jejuni</i> (21%) <i>H. influenzae</i> (8%) was present significantly...
We used the enzyme-linked immunosorbent assay to investigate autoantibodies against gangliosides GM1, GD1a, GD1b, GT1b, GD2, and GQ1b in sera from 16 patients with Fisher's syndrome. found high anti-GQ1b antibody titers, mainly those of IgG class, 13 these patients. The titers decreased clinical course illness. Moreover, antibody-positive had more severe ataxia cerebellar type than antibody-negative
Abstract Paranodal axo‐glial junctions are important for ion channel clustering and rapid action potential propagation in myelinated nerve fibers. Paranode formation depends on the cell adhesion molecules neurofascin (NF) 155 glia, a Caspr contactin heterodimer axons. We found that antibody to ganglioside GM1 labels paranodal regions. Autoantibodies gangliosides GD1a thought disrupt nodes of Ranvier peripheral motor nerves cause Guillain‐Barré syndrome, an autoimmune neuropathy characterized...
Molecular mimicry of Campylobacter jejuni lipo-oligosaccharides (LOS) with gangliosides in nervous tissue is considered to induce cross-reactive antibodies that lead Guillain-Barre syndrome (GBS), an acute polyneuropathy. To determine whether specific bacterial genes are crucial for the biosynthesis ganglioside-like structures and induction anti-ganglioside antibodies, we characterized C. LOS gene locus GBS-associated control strains. We demonstrated types associated GBS expression...
Molecular mimicry of Campylobacter jejuni lipo-oligosaccharides (LOS) with gangliosides in nervous tissue is considered to induce cross-reactive antibodies that lead Guillain-Barré syndrome (GBS), an acute polyneuropathy. To determine whether specific bacterial genes are crucial for the biosynthesis ganglioside-like structures and induction anti-ganglioside antibodies, we characterized C. LOS gene locus GBS-associated control strains. We demonstrated types associated GBS expression...