Immunoglobulins inhibit pathophysiological effects of anti-GQ1b-positive sera at motor nerve terminals through inhibition of antibody binding

Jacobs, B.C. (Bart); O'Hanlon, GM; Bullens, RW; Veitch, J.; Plomp, J. J.; Willison, H J

doi:10.1016/j.ajo.2003.11.031

Cited by 25 publications

(38 citation statements)

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“…It has previously been shown that immunoglobulins can attenuate in vitro deposition of complement factors, as well as reduce binding of IgG antibodies, leading to a reduced deposition of MAC. 8,45 Although our model shows a reduced deposition of MAC following preincubation of serum with immunoglobulins, this reduction is modest compared to the rescue of calcium homeostasis dysfunction. Furthermore, immunoglobulins rescue complement-independent effects of IgM anti-GM1 antibodies, pointing toward a direct modulatory effect of antibody binding or antiidiotype mechanism.…”

Section: Discussionmentioning

confidence: 82%

“…This mechanism has been previously shown to underlie pathogenicity of antiganglioside IgG antibodies at the neuromuscular junction and the distal nodes of Ranvier in ex vivo mouse models and the in vivo rabbit model. 3,32,[45][46][47] In these models, complement deposition caused calcium influxes that disrupted the cytoskeleton and the clustering of sodium channels. Our results suggest that lower affinity anti-GM1 IgM antibodies exert similar effects to IgG antibodies.…”

Section: Discussionmentioning

confidence: 99%

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Autoantibody pathogenicity in a multifocal motor neuropathy induced pluripotent stem cell–derived model

Harschnitz

Berg

Johansen

et al. 2016

Annals of Neurology

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Autoantibody pathogenicity in a multifocal motor neuropathy induced pluripotent stem cell–derived model

Harschnitz

Berg

Johansen

et al. 2016

Annals of Neurology

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“…5) The therapeutic effect of i.v. Ig (IVIg) in GBS patients is also partly due to the prevention of complement activation (12).…”

Section: G Uillain-barré Syndrome (Gbs)mentioning

confidence: 99%

Mannose-Binding Lectin Contributes to the Severity of Guillain-Barré Syndrome

Geleijns

Roos²,

Houwing-Duistermaat

et al. 2006

The Journal of Immunology

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In Guillain-Barré syndrome (GBS), complement activation plays a crucial role in the induction and extent of the postinfectious immune-mediated peripheral nerve damage. Mannose-binding lectin (MBL) activates the complement system via the lectin pathway after recognition of repetitive sugar groups on pathogens. We investigated whether the MBL2 genotype, serum MBL level, and MBL complex activity are associated with the development and severity of GBS. Single nucleotide polymorphisms in the promoter region (−550 H/L and −221 X/Y) and exon 1 (A/O) of the MBL2 gene were determined in 271 GBS patients and 212 healthy controls. The frequencies of the H allele, HY promoter haplotype, and HYA haplotype, which are related to high MBL activity, were all increased in GBS patients compared with healthy controls (p ≤ 0.03), particularly in severely affected GBS patients (MRC-sum score <40) (p ≤ 0.02). Severe weakness was also associated with high MBL concentrations and MBL complex activity in sera from GBS patients (p < 0.01). The MBL2 B allele was associated with functional deficiency and relatively mild weakness. These results support the hypothesis that complement activation mediated by MBL contributes to the extent of nerve damage in GBS, which is codetermined by the MBL2 haplotype.

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“…Plasmapheresis and IVIG are the main therapies for AIDP. Plasmapheresis removes circulating autoantibodies in the blood, while IVIG may neutralize autoantibodies (13) and prevent complement-mediated nerve damage (14).…”

Section: Discussionmentioning

confidence: 99%

Recurrent Acute Inflammatory Demyelinating Polyradiculoneuropathy Following R-Chop Treatment for Non-Hodgkin Lymphoma

Liang

Singh²,

Witzig³

2013

Baylor University Medical Center Proceedings

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Proc (Bayl Univ Med Cent) 2013;26(2):156-158Acute flaccid paralysis following chemotherapy has a wide differential diagnosis, including drug toxicity, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), and malignant nerve infiltration. We present a case of recurrent acute quadriparesis due to AIDP following chemotherapy for non-Hodgkin lymphoma, which resolved each time following administration of intravenous immunoglobulin. Although many chemotherapeutic agents can cause neurologic side effects, such as peripheral neuropathy, drug toxicity as a cause is a diagnosis of exclusion.A cute fl accid paralysis following chemotherapy has a wide diff erential diagnosis, including drug toxicity, acute infl ammatory demyelinating polyradiculoneuropathy (AIDP), and malignant nerve infi ltration. We present a case of recurrent acute quadriparesis due to AIDP following chemotherapy for non-Hodgkin lymphoma, which resolved each time following administration of intravenous immunoglobulin (IVIG). CASE PRESENTATIONA 62-year-old man with recently diagnosed stage IV diffuse large B-cell lymphoma presented for his fi rst cycle of chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Th e diagnosis had been confi rmed by pleural and testicular biopsies. Pretreatment positron emission tomography (PET) scan had revealed diff use nodal activity and extranodal involvement in the pleura, testicles, and bones (Figure 1a). Th e patient had been otherwise healthy.He tolerated his fi rst cycle of R-CHOP chemotherapy with no issues. Two days after completing the R-CHOP cycle, he began to notice bilateral lower-extremity weakness, which began at his feet and gradually moved upwards to his hip girdle muscles. Th e weakness gradually worsened to the point where he needed to use his hands to push off and stand from a seated position. Shortly thereafter, he noted bilateral arm weakness and became unable to stand due to the inability to push off with his arms. He also developed numbness in all four extremities from his mid forearms distally and the knees down. Th roughout this time, he retained bowel and bladder function. His severe weakness and

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Immunoglobulins inhibit pathophysiological effects of anti-GQ1b-positive sera at motor nerve terminals through inhibition of antibody binding

Cited by 25 publications

References 0 publications

Autoantibody pathogenicity in a multifocal motor neuropathy induced pluripotent stem cell–derived model

Autoantibody pathogenicity in a multifocal motor neuropathy induced pluripotent stem cell–derived model

Mannose-Binding Lectin Contributes to the Severity of Guillain-Barré Syndrome

Recurrent Acute Inflammatory Demyelinating Polyradiculoneuropathy Following R-Chop Treatment for Non-Hodgkin Lymphoma

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