Major platelet tasks in hemostasis and immunity. Platelets circulate in blood, surveying the vasculature for (A) hemostatic and (B) immune threats. (A) Platelets detect vascular breaches using a variety of receptors, such as those binding exposed collagen (1). They respond to danger signals such as ADP or the contents of Weibel-Palade (WP) bodies, released by damaged or activated endothelial cells (2). Upon activation, platelets can initiate thrombosis (3) while regulating vessel permeability (4). They also act as gatekeepers, physically preventing erythrocyte loss during leukocyte transmigration (5), and also at the lymphovenous junction at steady state or during lymphangiogenesis (6). (B) Platelets may recognize immune threats directly using evolutionarily conserved pattern receptors (1) or indirectly via leukocyte signals, such as neutrophil extracellular traps (NETs) or cytokines (2). Platelets can bind and wrap around pathogens, triggering degranulation to effect killing (3) and direct/indirect leukocyte recruitment (4). Additionally, platelets often physically interact with leukocytes to deliver or exchange signals that result in fully active inflammation, for example by taking up arachidonic acid (AA) from neutrophils to synthesize thromboxane A2 (TXA2; 5).
