Platelets mediate inflammatory monocyte activation by SARS-CoV-2 spike protein.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 34964720.
- Also identified by DOI 10.1172/JCI150101 and PMC identifier 8843740.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Infection with SARS-CoV-2, the causative agent of COVID-19, causes mild to moderate disease in most patients but carries a risk of morbidity and mortality. Seriously affected individuals manifest disorders of hemostasis and a cytokine storm, but it is not understood how these manifestations of severe COVID-19 are linked. Here, we showed that the SARS-CoV-2 spike protein engaged the CD42b receptor to activate platelets via 2 distinct signaling pathways and promoted platelet-monocyte communication through the engagement of P selectin/PGSL-1 and CD40L/CD40, which led to proinflammatory cytokine production by monocytes. These results explain why hypercoagulation, monocyte activation, and a cytokine storm are correlated in patients severely affected by COVID-19 and suggest a potential target for therapeutic intervention.
Medical subject headings
- Blood Platelets
- COVID-19
- Inflammation
- Monocytes
- SARS-CoV-2
- Spike Glycoprotein, Coronavirus