ReviewImmunity, inflammation and disease2026
The Complement System in ANCA-Associated Vasculitis: Mechanistic Insights, Therapeutic Horizons, and Unmet Clinical Needs.
Review in Immunity, inflammation and disease, 2026. 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.
- In Vivo Efficacy of an Inhibitor of Complement and FcRn in Models of Glomerulonephritis and Collagen-Induced Arthritis Using Human C2 Knock-In Mice.International journal of molecular sciences · 2026Article
- Article
- Article
- The Complement System in ANCA-Associated Vasculitis: Mechanistic Insights, Therapeutic Horizons, and Unmet Clinical Needs.Immunity, inflammation and disease · 2026Review
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2 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundANCA-associated vasculitides (AAV) are autoimmune small-vessel vasculitides characterized by necrotizing inflammation with few immune deposits ("pauci-immune" lesions). Historically, complement was thought to play a minor role in AAV due to scant complement deposition on biopsy. However, growing evidence from animal models and patient studies indicate that complement activation, particularly the alternative pathway, is a critical amplifier of inflammation in AAV.
methodsWe searched PubMed, Embase, and Web of Science (January 2000-October 2024) for peer-reviewed studies on complement in AAV prioritizing preclinical, clinical, and therapeutic research.
findingsComplement activation bridges innate and adaptive immunity in AAV: ANCA-activated neutrophils release factors that trigger the alternative complement pathway, generating C5a, which further recruits and primes neutrophils, creating a self-amplifying loop of inflammation. Complement components (C3a, C5a, C5b-9) are detectable in active AAV patients' plasma/urine and in affected tissues, correlating with disease activity and severity. Therapeutically, the C5a-receptor antagonist, avacopan has demonstrated clinical efficacy, achieving remission with reduced corticosteroid exposure.
conclusionComplement dysregulation is a pivotal mechanism in AAV pathogenesis, opening a new era of complement-targeted therapies. Avacopan's success illustrates the potential to improve outcomes and safety by modulating complement. Yet, major unmet clinical needs remain. Up to 50% of patients relapse within 5 years. There are no validated biomarkers to predict relapse. Long-term steroid dependence and cumulative toxicity from rituximab and cyclophosphamide compromise patient safety. Better tools are needed to detect early disease, stratify relapse risk, and personalize therapy. Future directions must prioritize biomarker development, novel complement inhibitors, and deliver durable remission with fewer side effects.
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