ArticleEuropean journal of neurology2025
Complement activation by IgM autoantibodies linked to immune-mediated neuropathies depends on C2.
Article in European journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Reducing sialylation in melanoma increases classical pathway-mediated complement activation.iScience · 2026Article
- Role of complement and complement-targeted therapeutics in neurological diseases.Nature reviews. Neurology · 2026Review
- IgM Anti-Ganglioside Binding and Complement Activation in an iPSC-Derived Motor Neuron Model for Multifocal Motor Neuropathy.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Complement activation by IgM autoantibodies linked to immune-mediated neuropathies depends on C2.European journal of neurology · 2025Article
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10 authors.
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Abstract
background and purposeComplement factor C2 is a potential therapeutic target in immune-mediated neuropathies. However, literature suggests that classical complement pathway activation may proceed to C3 in the absence of C2, a so-called "C2 bypass." Here, we evaluated a C2 bypass mechanism during complement activation by pathogenic human IgM from patients with immune-mediated neuropathies.
methodsIgM autoantibodies from 51 patients with multifocal motor neuropathy (MMN) or anti-myelin-associated glycoprotein (MAG) neuropathy (AMN) were used to activate complement in ex vivo disease models. C2 bypass was evaluated using C2-depleted (C2D) serum and a therapeutic anti-C2 antibody.
resultsIn two different disease models of MMN, IgM anti-GM1 and IgM anti-GM2 autoantibodies from MMN patients were bound to induced pluripotent stem cell-derived motor neurons and Schwann cells, respectively, and fixed C3 upon incubation with fresh serum. C3 fixation was inhibited by anti-C2 and did not occur with C2D serum. Similarly, in an AMN model, IgM anti-MAG antibodies were incubated with fresh serum fixed C3, which in all cases was abrogated in the absence of C2 or in the presence of anti-C2.
conclusionsIn ex vivo disease models of MMN and AMN, complement activation by IgM autoantibodies from 51 patients was in all cases dependent on C2 and was inhibited by an antihuman C2 antibody. No evidence of a C2 bypass mechanism was found.
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