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Antibodies to chondroitin sulfate C: a new detection assay and correlations with neurological diseases
Antibodies to chondroitin sulfate C (ChS C) have been previously associated with sensory axonal neuropathy. Investigation of these antibodies has, however, been limited by the lack of a sensitive and reliable test for their detection. We developed a new enzyme-linked immunoassorbent assay (ELISA), where biotinylated ChS C was made to adhere to avidin-coated microwells. The new ELISA showed a much greater sensitivity than other currently available ELISAs for detection of anti-ChS C antibodies. A total of 480 sera (466 patients and 14 normal volunteers) were tested at increasing dilutions for anti-ChS C antibody activity. Normal subjects had IgM anti-ChS C antibody titers of up to 3,200 and mildly elevated titers of 6,400 were seen in a variety of diseases. Eleven patients had titers of 12,800 or higher. These included seven patients with sensory axonal neuropathy, three with amyotrophic lateral sclerosis and one with corticobasal ganglionic degeneration. These studies indicate that anti-ChS antibodies do occur in patients with axonal sensory neuropathy, but are not limited to that disease
Anti-MAG antibody and antibody complexes: detection by radioimmunoassay
A radioimmunoassay (RIA) for measuring isotype-specific antibodies to the myelin-associated glycoprotein (MAG) was developed using radiolabeled CNS MAG in a double-antibody precipitation system. Anti-MAG activity was detected by RIA only in patients with neuropathy and anti-MAG M proteins. Anti-MAG IgM or IgG antibodies were not detected in serum of patients with Guillain-Barré syndrome, chronic relapsing polyneuritis, or multiple sclerosis (MS). Some patients with anti-MAG IgM M proteins also had complexes of IgG or IgA bound to the M protein. In one patient, anti-CNS MAG activity was detected by RIA, but not by ELISA or immunoblot. Anti-MAG antibody activity in patients with neuropathy seems to be isotypically restricted, and there is no evidence for antibody reactivity to MAG in other demyelinating diseases
Antibodies to Chondroitin Sulfates A, B, C: clinico-pathological correlates in neurological diseases
Anti-chondroitin sulfates (ChSs) antibodies have been reported in neuropathy and neurodegenerative diseases. Differences in specificities may account for their association with different diseases. Sera from 303 neurological patients were tested for antibodies to ChSs A, B, C. Titers >/=51,200 were found in 16 patients (eight peripheral neuropathy, three motor neuron disease, four multiple sclerosis, one myelitis). Three patients also had anti-sulfatides antibodies, which in two cases cross-reacted with ChSs. By indirect immunofluorescence, positive sera stained nuclei on normal human peripheral nerve sections. These findings indicate that human anti-ChSs antibodies are broadly reactive and not specific to any neurological disease
Specificity of human M-proteins that bind to myelin associated glycoprotein : peptide mapping, deglycosylation and competitive binding studies
Conduction abnormalities induced by sera of patients with multifocal motor neuropathy and anti‐GM1 antibodies
Increased titers of anti‐GM1 antibodies have been associated with motor neuron disease and motor neuropathy with or without conduction block. To investigate the pathogenetic role of anti‐GM1 antibodies we injected into rat tibial nerves sera from patients with multifocal motor neuropathy and conduction block (MMN) or progressive spinal muscular atrophy (PMA), both presenting anti‐GM1 antibodies. Sera of patients with MMN produced reduction of amplitude and dispersion of compound muscle action potential from proximal stimulation. Morphometry revealed demyelination in 6.2% of fibers. Sera of patients with PMA did not produce clear‐cut electrophysiological or morphological changes. Differential effects of sera from patients presenting high‐titer anti‐GM1 antibodies, but with distinct clinical syndromes, might depend on differences in anti‐GM1 antibody affinity, valency, or ability to fix complement. Alternatively, circulating factors other than, or in addition to, anti‐GM1 antibodies present in sera of patients with MMN, but not of PMA patients, might be responsible for conduction abnormalities and reproduce them after passive transfer. © 1993 John Wiley & Sons, Inc. Copyright © 1993 John Wiley & Sons, Inc
Keyhole limpet hemocyanin contains Gal(?1-3)-GalNAc determinants that are cross-reactive with the T-antigen
Keyhole limpet hemocyanin (KLH) is widely used as a carrier molecule to enhance immune responses to administered antigens, and for immunotherapy of bladder and renal carcinoma. In the present study we show, using lectin and antibody binding studies, that native KLH contains Gal(beta 1-3)GalNAc-bearing oligosaccharides, and that immunization with KLH in Lewis rats induces the production of anti-Gal(beta 1-3) GalNAc antibodies. This might explain the beneficial effect of KLH in bladder cancers that express cross-reactive Gal(beta 1-3)GalNAc determinants or the T antigen
Anti-MAG antibodies and antibody complexes in patients with peripheral neuropathy and IgM M-protein
Correction: Latov, N. Campylobacter jejuni Infection, Anti-Ganglioside Antibodies, and Neuropathy. Microorganisms 2022, 10, 2139
The authors wish to make the following corrections to this paper [...
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