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Complement profiling of sural nerves in chronic-inflammatory demyelinating polyneuropathy.

Frauke Stascheit1,2, Andreas Roos3,4,5, Christina B Schroeter3

  • 1Charité-Universitätsmedizin Berlin, Department of Neurology With Experimental Neurology, Corporate Member of Freie Universität Berlin and Humboldt Universität Zu Berlin, Charitéplatz 1, 10117, Berlin, Germany. frauke.stascheit@charite.de.

Acta Neuropathologica
|September 19, 2025
PubMed
Summary

Complement complex C5b-9 deposition is prevalent in chronic-inflammatory demyelinating polyneuropathy (CIDP) nerve biopsies, correlating with disease severity. This finding supports complement-targeted therapies for CIDP patients.

Keywords:
Chronic-inflammatory demyelinating polyneuropathyComplement profilesGene expressionProteomicsSural nerve

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Area of Science:

  • Neurology
  • Immunology
  • Pathology

Background:

  • Chronic-inflammatory demyelinating polyneuropathy (CIDP) is a rare, disabling immune-mediated disorder.
  • The role of the complement system in CIDP pathogenesis is not well understood.
  • Understanding complement's role is crucial given the development of complement-targeted treatments.

Purpose of the Study:

  • To investigate the involvement of the complement system in the sural nerve pathology of CIDP patients.
  • To correlate complement deposition with clinical disease severity and immune cell infiltration.

Main Methods:

  • Sural nerve biopsies from 55 CIDP patients, 2 non-diseased controls (NDCs), and 8 patients with hereditary neuropathy (HN) or idiopathic axonal neuropathy (IPN) were analyzed.
  • Histopathology, gene expression, and proteomics were employed to assess complement deposition and related molecular changes.
  • Immunohistochemistry was used to quantify CD8+ T cells and CD68+ macrophages.

Main Results:

  • Prominent deposition of terminal complement complex C5b-9 was observed in endoneurial capillaries of 94% of CIDP patients.
  • Significant complement deposition correlated with a progressive disease course and infiltration of CD8+ T cells and CD68+ macrophages.
  • The extent of immune cell infiltration correlated with clinical disease severity (INCAT score, p < 0.001).

Conclusions:

  • This study demonstrates significant complement involvement in CIDP nerve pathology, supporting the concept of complement-mediated demyelination.
  • The findings suggest that targeting the complement system could be a promising therapeutic strategy for a subset of CIDP patients.
  • Further research is needed to elucidate the functional role of complement in CIDP progression and optimize patient management.