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ABSTRACT: Demyelination of feline sciatic nerve was induced by intraneural injection of serum from three patients with neuropathy and an IgM M-protein that reacted with myelin-associated glycoprotein (MAG). Demyelination exceeded that induced by serum from 18 other individuals, including six IgM M-proteins unreactive with MAG. The myelinolytic effect required active human complement and was abolished by exposure of serum to homogenate of human peripheral nerve that removed 90% of the M-protein. Immunofluorescence studies demonstrated deposition of the injected M-protein and complement on the surface of myelin sheaths, implying that the M-protein reacted with epitopes of myelin exposed to the extracellular space.
Neurology 03/1987; 37(2):242-56. · 8.31 Impact Factor
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ABSTRACT: Immunofluorescence histochemistry was used to study the pathogenesis of polyneuropathy in patients with an IgM M protein. Seventeen patients had an M protein that reacted with myelin-associated glycoprotein (MAG), and their serum immunostained myelin sheaths of normal peripheral nerve of humans and certain other species. The staining was specific for the M protein idiotype and was abolished by prior absorption of serum with MAG. The sural nerve biopsy specimens from these 17 patients had pathological features of primary demyelination and deposits of IgM on the myelin sheaths. Sural nerve specimens of 2 patients with an M protein reactive with chondroitin sulfate showed axonal degeneration and diffuse deposits of IgM in the endoneurium. Serum of one of these patients immunostained connective tissue; the staining was specific for the M protein idiotype and was blocked by absorption of the serum with chondroitin sulfate. The antigenic specificity of the IgM M protein in another 9 patients with neuropathy is not known; however, sural nerve specimens obtained from some of the patients showed axonal degeneration and endoneurial deposits of IgM, and the serum IgM immunostained axons in some instances. The findings suggest that IgM M proteins may cause the neuropathy and that more than one autoantigen is involved.
Annals of Neurology 09/1985; 18(2):173-81. · 11.09 Impact Factor
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ABSTRACT: Anti-MAG IgM antibodies were detected by ELISA in a patient with slowly progressive peripheral neuropathy. Serum IgM content was normal, and no M-protein was detected by serum protein electrophoresis, immunoelectrophoresis, or immunostaining. By immunoblot analysis, the anti-MAG antibodies were IgMk; they reacted with human and bovine MAG but not with mouse MAG. The data suggest that there was an anti-MAG IgM M-protein in concentration too low to be detected by conventional techniques. Tests for anti-MAG antibodies should be done in patients with slowly progressive neuropathy of unknown etiology, even in the absence of detectable serum M-protein.
Neurology 03/1984; 34(2):218-21. · 8.31 Impact Factor
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Journal of Neuropathology and Experimental Neurology 04/1983; 42(3):349. · 4.26 Impact Factor
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ABSTRACT: We studied two patients with an axonal type of polyneuropathy, epidermolysis, and IgM kappa plasma cell dyscrasia. The IgM kappa was deposited in the dermis, was absorbed from the serum by axonal micelle preparations, and was precipitated with chondroitin sulfate in highly purified agarose in 0.15 M NaCl with 0.01 M phosphate buffer, pH 7.8. In contrast, we found none of these abnormalities in three patients with IgM plasma cell dyscrasia and demyelinating neuropathy. Of 78 other macroglobulinemic serum samples from patients without neuropathy, 7 precipitated with a sulfated polysaccharide. This reaction occurred at low ionic strength, 0.05 M barbital buffer, pH 8.1, but did not occur in the higher ionic strength of 0.01 M phosphate with 0.15 M NaCl (PBS). The interaction of the IgM with chondroitin sulfate at relatively high ionic strength could cause both the axonal polyneuropathy and the epidermolysis.
Neurology 03/1983; 33(2):192-201. · 8.31 Impact Factor
