Monoclonal IgM from patients with peripheral demyelinating neuropathies cross‐react with bacterial polypeptides

SUMMARY Human monoclonal IgM associated with a demyelinating peripheral neuropathy often feature a distinct antibody activity directed against a glucuronyl sulphate epitope shared by myelin‐associated glycoprotein (MAG), nerve glycolipids and low molecular weight peripheral nerve polypeptides‐ Earli...

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Bibliographic Details
Published in:Clinical and experimental immunology 1994-06, Vol.96 (3), p.466-469
Main Authors: BROUET, J.‐C., MARIETTE, X., GENDRON, M.‐C., DUBREUIL, M.‐L.
Format: Article
Language:English
Subjects:
Antibodies, Bacterial - immunology
Antibodies, Monoclonal - immunology
antibody activity of monoclonal IgM
Antigens, Bacterial - immunology
Autoantibodies - immunology
Autoantigens - immunology
bacterial extracts
Bacterial Proteins - immunology
Cross Reactions
Demyelinating Diseases - etiology
Demyelinating Diseases - immunology
Humans
Immunoglobulin M - immunology
lymphoplasmacytic proliferation
myelin‐associated glycoprotein
peripheral neuropathy
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Summary:SUMMARY Human monoclonal IgM associated with a demyelinating peripheral neuropathy often feature a distinct antibody activity directed against a glucuronyl sulphate epitope shared by myelin‐associated glycoprotein (MAG), nerve glycolipids and low molecular weight peripheral nerve polypeptides‐ Earlier studies showed that these IgM use a diverse repertoire of VH, and VL genes which exhibit somatic mutations, possibly indicative of an antigen‐driven process. Here, we investigated whether such monoclonal IgM may react with environmental bacterial antigens. We found that six patients' sera and purified monoclonal IgM, as well as IgM from supernatants of three clonal anti‐MAG‐secreting cell lines reacted with unique 90 ‐100kD polypeptides from extracts of two out of 10 bacterial species. Purified MAG was able to inhibit this reactivity. These results indicate molecular mimicry as a possible mechanism of this immunomediated neuropathy and associated clonal lymphoid disease.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.1994.tb06052.x