作者
Dimitrios C Mastellos, Bruno GP Pires da Silva, Benedito AL Fonseca, Natasha P Fonseca, Maria Auxiliadora-Martins, Sara Mastaglio, Annalisa Ruggeri, Marina Sironi, Peter Radermacher, Akrivi Chrysanthopoulou, Panagiotis Skendros, Konstantinos Ritis, Ilenia Manfra, Simona Iacobelli, Markus Huber-Lang, Bo Nilsson, Despina Yancopoulou, E Sander Connolly, Cecilia Garlanda, Fabio Ciceri, Antonio M Risitano, Rodrigo T Calado, John D Lambris
发表日期
2020/11/1
期刊
Clinical Immunology
卷号
220
页码范围
108598
出版商
Academic Press
简介
Growing clinical evidence has implicated complement as a pivotal driver of COVID-19 immunopathology. Deregulated complement activation may fuel cytokine-driven hyper-inflammation, thrombotic microangiopathy and NET-driven immunothrombosis, thereby leading to multi-organ failure. Complement therapeutics have gained traction as candidate drugs for countering the detrimental consequences of SARS-CoV-2 infection. Whether blockade of terminal complement effectors (C5, C5a, or C5aR1) may elicit similar outcomes to upstream intervention at the level of C3 remains debated. Here we compare the efficacy of the C5-targeting monoclonal antibody eculizumab with that of the compstatin-based C3-targeted drug candidate AMY-101 in small independent cohorts of severe COVID-19 patients. Our exploratory study indicates that therapeutic complement inhibition abrogates COVID-19 hyper-inflammation. Both …
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DC Mastellos, BGPP da Silva, BAL Fonseca… - Clinical Immunology, 2020