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The first case of COVID-19 treated with the complement C3 inhibitor AMY-101.
Clinical Immunology ( IF 8.6 ) Pub Date : 2020-04-29 , DOI: 10.1016/j.clim.2020.108450
Sara Mastaglio 1 , Annalisa Ruggeri 1 , Antonio M Risitano 2 , Piera Angelillo 1 , Despina Yancopoulou 3 , Dimitrios C Mastellos 4 , Markus Huber-Lang 5 , Simona Piemontese 1 , Andrea Assanelli 1 , Cecilia Garlanda 6 , John D Lambris 7 , Fabio Ciceri 8
Affiliation  

Acute respiratory distress syndrome (ARDS) is a devastating clinical manifestation of COVID-19 pneumonia and is mainly based on an immune-driven pathology. Mounting evidence suggests that COVID-19 is fueled by a maladaptive host inflammatory response that involves excessive activation of innate immune pathways. While a "cytokine storm" involving IL-6 and other cytokines has been documented, complement C3 activation has been implicated as an initial effector mechanism that exacerbates lung injury in preclinical models of SARS-CoV infection. C3-targeted intervention may provide broader therapeutic control of complement-mediated inflammatory damage in COVID-19 patients. Herein, we report the clinical course of a patient with severe ARDS due to COVID-19 pneumonia who was safely and successfully treated with the compstatin-based complement C3 inhibitor AMY-101.

中文翻译:

第一例用补体C3抑制剂AMY-101治疗的COVID-19。

急性呼吸窘迫综合征(ARDS)是COVID-19肺炎的毁灭性临床表现,主要基于免疫驱动的病理学。越来越多的证据表明,COVID-19由适应不良的宿主炎症反应推动,该炎症反应涉及先天免疫途径的过度激活。尽管有文献报道涉及IL-6和其他细胞因子的“细胞因子风暴”,但在SARS-CoV感染的临床前模型中,补体C3的激活被认为是加剧肺损伤的初始效应器机制。以C3为靶点的干预措施可能为COVID-19患者的补体介导的炎症损伤提供更广泛的治疗控制。在这里
更新日期:2020-04-29
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