Complement as a target in COVID-19?
Antonio M. Risitano, Dimitrios C. Mastellos, Markus Huber-Lang, Despina Yancopoulou, Cecilia Garlanda, Fabio Ciceri & John D. Lambris
Nature Reviews Immunology (2020)
There is an urgent need to develop effective therapies for COVID-19. Here, we urge immunologists and clinicians to consider the potential of targeting the complement system in these patients.
Most patients who become critically ill following infection with SARS-CoV-2, the causative agent of COVID-19, develop acute respiratory distress syndrome (ARDS)1. The deterioration of lung function has been attributed to a maladaptive immune response rather than increased viral loads. One theory is that the activation of lung-resident immune cells via pattern-recognition receptors drives the release of pro-inflammatory cytokines and extravasation of blood neutrophils and monocytes into the bronchi. These cells may disrupt the air–blood barrier by causing collateral tissue damage, particularly to airway epithelial cells and vascular endothelial cells, which express the ACE2 entry receptor for SARS-CoV-2; the damage of vascular endothelial cells may account for thrombotic microangiopathies.
