原文开头
Heterogeneous blood clots rich in activated and procoagulant platelets, fibrin, and red blood cells form on the endothelium of blood vessels at sites of inflammation and infection. Activated platelets support neutrophil recruitment and activation, and the formation of NETs, which are webs of DNA, histones, and antimicrobial proteins that trap and kill harmful bacteria. In acute severe infection, platelets can also adhere to VWF and fibrin at sites of inflammation, in a process that is blood-flow dependent. Two platelet proteins, the integrin αIIbβ3 and the tetraspanin CD9, cluster on tethers called PITTs on the endothelium and on neutrophils. The main body of the platelet detaches and reenters the circulation in a hyporesponsive state, which might increase bleeding risk. …
摘自《科学》(Science)第391卷 第6783期 · 2026年1月22日。仅引用开头一小段供了解文章,版权归原刊所有,全文请阅读原刊。