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Monoclonal IgM from patients with peripheral demyelinating neuropathies cross-react with bacterial polypeptides
J C Brouet1, X Mariette, M C Gendron
1Department of Cytofluorometry, Hôpital Saint-Louis, Paris, France.
Clinical and Experimental Immunology
|June 1, 1994
Summary
Human IgM antibodies linked to demyelinating neuropathy may target bacterial antigens, suggesting molecular mimicry. This immune response could explain nerve damage and associated lymphoid diseases.
Area of Science:
- Neuroimmunology
- Molecular mimicry
- Peripheral neuropathies
Background:
- Monoclonal IgM antibodies are associated with demyelinating peripheral neuropathies.
- These antibodies often target the glucuronyl sulfate epitope on myelin-associated glycoprotein (MAG) and other nerve components.
- Previous research indicated antigen-driven selection of antibody genes.
Purpose of the Study:
- To investigate if monoclonal IgM antibodies in demyelinating neuropathy cross-react with environmental bacterial antigens.
- To explore the role of molecular mimicry in the pathogenesis of these neuropathies.
Main Methods:
- Analysis of patient sera and purified monoclonal IgM for reactivity against bacterial extracts.
- Testing IgM from anti-MAG-secreting cell lines.
- Inhibition assays using purified MAG to confirm specificity.
Main Results:
- Six patient sera and purified IgM, plus IgM from cell lines, reacted with bacterial polypeptides (90-100 kD) from two of ten bacterial species.
- Reactivity was inhibited by purified MAG, confirming cross-reactivity.
- Identified specific bacterial antigens potentially involved in the immune response.
Conclusions:
- Molecular mimicry between bacterial antigens and nerve components is a likely mechanism in IgM-associated demyelinating peripheral neuropathy.
- This cross-reactivity may trigger the autoimmune response leading to nerve damage.
- Suggests a potential link between environmental factors and autoimmune neuropathies.