Evidence map›Paper›PMID 39571136›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2025

The Role of Complement Activation in IgM M-Protein-Associated Neuropathies.

Johannes P M van de Mortel, Kevin Budding, Kim Dijkxhoorn, Monique C Minnema, Alexander F J E Vrancken, Nicolette C Notermans, W Ludo van der Pol, IMAGiNe Consortium

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In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. High-Throughput BLI for One-Step Anti-International journal of molecular sciences · 2026
    Article
  3. N-Glycan-Dependent Proinflammatory Effects of IgM in Anti-MAG Neuropathy.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Article
  4. Article
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Johannes P M van de MortelFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.ORCID 0000-0002-9956-744X
Kevin BuddingFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.
Kim DijkxhoornFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.ORCID 0009-0005-9692-9360
Monique C MinnemaFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.ORCID 0000-0002-3139-8379
Alexander F J E VranckenFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.
Nicolette C NotermansFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.ORCID 0000-0002-9363-4103
W Ludo van der PolFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.
IMAGiNe ConsortiumFrom the Department of Neurology and Neurosurgery (J.P.M.M., A.F.J.E.V., N.C.N., W.L.v.d.P.), UMC Utrecht Brain Center; Center for Translational Immunology (K.B., K.D.); Department of Hematology (M.C.M.), University Medical Center Utrecht, Utrecht University, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesPolyneuropathy associated with an immunoglobulin M (IgM) monoclonal gammopathy is characterized by slowly progressive, predominantly distal sensorimotor deficits, sensory ataxia, and electrophysiologic features of demyelination. IgM antibodies against myelin-associated glycoprotein (MAG) are present in serum from most patients. Nerve damage most likely results from the concerted action of binding of anti-MAG antibodies to nerves, followed by complement activation. The interaction of anti-MAG antibodies with complement activation and their relation to clinical characteristics have not been studied in detail. We studied the correlation among anti-MAG antibody titers, complement activation, and IgM-associated polyneuropathy disease severity.

methodsWe used serum samples from 101 patients with IgM-associated polyneuropathy to assess IgM anti-MAG titers by ELISA and antibody-mediated complement deposition using both an ELISA-based system and a cell-based system of primate peripheral nerve slides. We studied correlations of complement activation with anti-MAG ELISA titers and clinical characteristics.

resultsIgM anti-MAG titers varied from negative to strongly positive. Complement deposition in the ELISA-based system correlated significantly with anti-MAG antibody titer (Spearman rho 0.80; DISCUSSION: Anti-MAG antibody titers correlate with the level of complement activation in both ELISA and cell-based systems. However, clinical characteristics of IgM-associated polyneuropathy do not or only weakly correlate with titers or the level of complement deposition. The lack of clear correlations between complement activation and clinical characteristics does, at this stage, not support the use of complement inhibitors in the treatment of IgM-associated polyneuropathy.

Indexed as

Complement ActivationImmunoglobulin MMyelin-Associated GlycoproteinPolyneuropathiesAdultAgedAged, 80 and overAnimalsAutoantibodiesFemaleHumansMaleMiddle AgedParaproteinemiasAutoantibodiesImmunoglobulin MMAG protein, humanMyelin-Associated Glycoprotein

Identifiers

PMID39571136
PMCPMC11587989

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