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Complement C3-Targeted Therapy: Replacing Long-Held Assertions with Evidence-Based Discovery
Journal article   Open access   Peer reviewed

Complement C3-Targeted Therapy: Replacing Long-Held Assertions with Evidence-Based Discovery

Dimitrios C Mastellos, Edimara S Reis, Daniel Ricklin, Richard J Smith and John D Lambris
Trends in immunology, Vol.38(6), pp.383-394
06/2017
DOI: 10.1016/j.it.2017.03.003
PMCID: PMC5447467
PMID: 28416449
url
https://doi.org/10.1016/j.it.2017.03.003View
Published (Version of record) Open Access

Abstract

Complement dysregulation underlies several inflammatory disorders, and terminal complement inhibition has thus far afforded significant clinical gains. Nonetheless, emerging pathologies, fueled by complement imbalance and therapy-skewing genetic variance, underscore the need for more comprehensive, disease-tailored interventions. Modulation at the level of C3, a multifaceted orchestrator of the complement cascade, opens up prospects for broader therapeutic efficacy by targeting multiple pathogenic pathways modulated by C3-triggered proinflammatory crosstalk. Notably, C3 intervention is emerging as a viable therapeutic strategy for renal disorders with predominantly complement-driven etiology, such as C3 glomerulopathy (C3G). Using C3G as a paradigm, we argue that concerns about the feasibility of long-term C3 intervention need to be placed into perspective and weighed against actual therapeutic outcomes in prospective clinical trials. Proteins of the complement cascade together form a key innate immune sensor that mediates immunosurveillance and tissue homeostasis through extensive crosstalk with other pattern recognition systems. However, deregulation of complement responses can fuel a vicious cycle of tissue injury and inflammation. C5 blockade has proven effective for treating some complement-mediated diseases, but it has also revealed new pathogenic mechanisms that remain unaddressed. C3G is a rare renal disorder driven by aberrant complement activation and dysregulation of complement responses on the glomerular basement membrane (GBM). Blockade of the central component C3 is emerging as a therapeutic modality for C3G. Assertions related to potential risks and complications during prolonged C3 intervention need to be replaced by evidence-based discovery and clinical data.
anti-C5 therapy compstatin clinical efficacy C3 inhibitors C3 glomerulopathy AMY-101

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