ArticleJournal of neurology2025
Complement activation profiles in patients with immune checkpoint inhibitor-associated neuromuscular immune-related adverse events.
Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Role of complement and complement-targeted therapeutics in neurological diseases.Nature reviews. Neurology · 2026Review
- Muscle expression of PD1 and PD-L1 may predict the severity and outcomes of neuromuscular immune-related adverse events caused by immune checkpoint inhibitor treatment.Clinical rheumatology · 2026Article
- Emergency use of eculizumab in impending and manifest myasthenic crisis: a retrospective case series.Therapeutic advances in neurological disorders · 2026Article
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17 authors.
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Abstract
backgroundImmune-related neuropathy (irNeuropathy) and myositis (irMyositis) are the most common neurologic adverse events (irAE-n) associated with immune checkpoint inhibitors. Although case reports suggest benefits of complement inhibitors, the role of complement activation in irAE-n is understudied.
methodsIn a retrospective multicenter study, we enrolled patients with irNeuropathy or irMyositis, cancer controls (CCs), and healthy controls (HCs). Serum levels of 11 complement components were measured using multiplex enzyme-linked immunosorbent assays. Associations with irAE-n severity and outcomes were assessed by Spearman's correlation. C5b-9-positive complement deposition was analyzed in muscle and nerve specimens from a subset of patients.
resultsThirty-one irMyositis patients, 25 irNeuropathy patients, 25 CCs, and 17 HCs were included. Complement component levels were elevated in irNeuropathy (C3a, C5a, sC5b-9, C3, Ba, C4a), irMyositis (C3a, Ba), and CCs (C3a, C5a, sC5b-9, Bb, Ba, C4a), compared to HCs. In irMyositis, higher levels of C5a and complement regulators Factor H and I correlated with lower irAE-n severity (p = 0.02, rho = -0.45; p = < 0.01, rho = -0.56; p = < 0.001, rho = -0.67, respectively), and improved outcomes (p = 0.03, rho = -0.42; p = 0.05, rho = -0.40; p = < 0.001, rho = -0.64, respectively). Subtle C5b-9 deposition was detected in all tissue samples but showed non-specific patterns. DISCUSSION: Systemic complement activation is detectable in cancer patients regardless of irAE-n status, and tissue complement deposition is unspecific. Our findings suggest that complement activation is not a major driver of irAE-n, leaving the therapeutic potential of complement inhibitors uncertain.
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