Open AccessMonoclonal IgM from patients with peripheral demyelinating neuropathies cross‐react with bacterial polypeptides
Author(s) -
BROUET J.C.,
MARIETTE X.,
GENDRON M.C.,
DUBREUIL M.L.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06052.x
Subject(s) - epitope , antigen , monoclonal antibody , molecular mimicry , monoclonal , immunology , myelin , myelin associated glycoprotein , biology , cd5 , immunoglobulin m , antibody , immunoglobulin g , central nervous system , neuroscience
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 V H , and V L 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.