Gangliosides GM1 and GD1b are antigens for IgM M-protein in a patientwith motor neuron disease

Freddo, Lorenza; Yu, Robert K.; Latov, N.; Donofrio, Peter D.; Hays, Arthur P.; Greenberg, Harry S.; Albers, James W.; Allessi, A G; Keren, David F.

doi:10.1212/wnl.36.4.454

Cited by 207 publications

(55 citation statements)

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“…Antibody binding at these sites appears to be largely due to reactivity with GM1, rather than with other cross-reactive glycoproteins or glycolipids such as GDlb, because of the following reasons: (1) The intensity of immunostaining was proportional to the anti-GM1 antibody titers; (2) antibodies that were specific to GM1 exhibited the same pattern of reactivity; (3) the motor neurons were immunostained by CT, which is specific for GM1; and (4) anti-GM1 antibody binding to gray matter and motor neurons was specifically blocked by preincubation with CT, which does not bind to GDlb or glycoproteins. These findings are consistent with the observation that GM1 is the only common antigen found in patients with motor nerve disease and antiglycolipid antibodies [11][12][13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

Patterns of reactivity of human anti‐GM1 antibodies with spinal cord and motor neurons

Corbo

Quattrini

Lugaresi

et al. 1992

Annals of Neurology

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Human anti-GM1 antibodies from patients with lower motor neuron disease or predominantly motor neuropathy recognize carbohydrate determinants shared by GM1 and related glycolipids and glycoproteins, but the identity of the antigens to which they bind in tissue is unknown. We examined the binding of anti-GM1 antibodies with differing fine specificities to spinal cord, isolated motor neurons, and dorsal root ganglia neurons in order to characterize the tissue antigens. All anti-GM1 antibodies tested bound to the surface of bovine spinal motor neurons and immunostained the gray matter of unfixed sections of spinal cord. The staining was blocked by cholera toxin, which is specific for GM1, indicating that GM1 itself was the target antigen. Binding to white matter was more variable and depended on fixation and the fine specificities of the antibodies. The anti-GM1 antibodies did not bind to dorsal root ganglia neurons in tissue sections or in culture. These studies suggest that the autoantibodies might exert their effect, in part, by binding to GM1 on the surface of motor neurons, and that the absence of binding to dorsal root ganglia neurons might explain the lack of sensory abnormalities in affected patients.

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Section: Discussionmentioning

confidence: 99%

Patterns of reactivity of human anti‐GM1 antibodies with spinal cord and motor neurons

Corbo

Quattrini

Lugaresi

et al. 1992

Annals of Neurology

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“…Another pos sibility is that antibodies may arise secondary to the destruction of neuronal components. Freddo et al [3] reported a patient with MND-associated IgM parapro teinemia who antibodies to GM1 and GDlb and sug gested that antibodies may play a role in the disease. Shy et al [ 14] reviewed MND with monoclonal or polyclonal paraproteinemia and showed a significnatly higher inci dence of paraproteinemia in MND than in controls and improvement in some cases by immunosuppressive ther apy.…”

Section: Discussionmentioning

confidence: 99%

“…In patients with MND-associated IgM para proteinemia, the presence of antibodies to glycolipid has been demonstrated [3]. We searched for specific anti bodies to human spinal-cord proteins in sera from pa tients with MND and other neurological diseases.…”

Section: Introductionmentioning

confidence: 99%

Antibodies to Human Spinal Cord Proteins in Sera from Patients with Motor Neuron Disease and Other Neurological Diseases

Ishii

Sato²,

Yanagisawa³

et al. 1989

Eur Neurol

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Antibodies to human spinal-cord proteins in sera from patients with motor neuron disease (MND) and other neurological diseases were detected by the immunoblotting method. IgG in serum from a patient with amyotrophic lateral sclerosis reacted with insoluble proteins in the crude nuclear subfraction but the IgG in serum from other patients reacted with soluble proteins. The molecular weights of the antigens on the blots differed among the cases. The significance of the antibodies to neural tissue in sera from MND remains unknown. The etiology of MND is thought to be heterogenous and some types of MND may be closely related to humoral immunity.

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“…This is also true for analysis of the cerebrospinal fluid which, in most cases, shows a discrete increase in overall protein concentration (up to 80 mg/dl) but normal cell counts [108]. Serum electrophoresis might reveal elevated polyclonal antibody formation, while monoclonal peaks typical for IgM gammopathy are generally absent [4,109]. …”

Section: Diagnostics Of Mmnmentioning

confidence: 99%

Multifocal Motor Neuropathy: Update on Clinical Characteristics, Pathophysiological Concepts and Therapeutic Options

Meuth¹,

Kleinschnitz²

2010

Eur Neurol

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Multifocal motor neuropathy (MMN) is an acquired immune-mediated neuropathy characterized by chronic or stepwise progressive asymmetrical limb weakness without sensory deficits. The upper extremities are more often affected than the lower extremities with distal paresis dominating over proximal paresis. Important diagnostic features are persistent multifocal partial conduction blocks (CBs) and the presence of high-titer anti-GM1 serum antibodies. Motor neuron disease, other chronic dysimmune neuropathies, such as chronic inflammatory demyelinating polyneuropathy and the Lewis-Sumner syndrome (MADSAM neuropathy), are important differential diagnoses. While corticosteroids and plasma exchange are largely ineffective, high-dose intravenous immunoglobulins are regarded as first-line treatment. In spite of significant success in elucidating the underlying disease mechanisms in MMN during the past few years, important pathophysiological issues and the optimum long-term therapy remain to be clarified. The present review summarizes the clinical picture and current pathophysiological concepts of MMN with a special focus on the molecular and electrophysiological basis of CBs and highlights established therapies as well as possible novel treatment options.

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Gangliosides GM1 and GD1b are antigens for IgM M-protein in a patientwith motor neuron disease

Cited by 207 publications

References 0 publications

Patterns of reactivity of human anti‐GM1 antibodies with spinal cord and motor neurons

Patterns of reactivity of human anti‐GM1 antibodies with spinal cord and motor neurons

Antibodies to Human Spinal Cord Proteins in Sera from Patients with Motor Neuron Disease and Other Neurological Diseases

Multifocal Motor Neuropathy: Update on Clinical Characteristics, Pathophysiological Concepts and Therapeutic Options

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