Platelet receptors for the complement component C1q: implications for hemostasis and thrombosis.

Platelets participate in a variety of responses of the blood to injury (1). In addition to their well known role in hemostasis and thrombosis, platelets play a role in inflammation and react with components of the immune system. Immune complexes and aggregated IgG, for example, are known to activate platelets via ligation of Fc gamma RII receptors and induce the release of platelet granule contents, including biogenic amines and adenine nucleotides (2). Platelets also interact with the complement subcomponent C1q utilizing binding sites that are unrelated to C1s, a complement subcomponent which was originally suggested to support C1q binding to thrombocytes (3). The physiologic and pathologic consequences of platelet C1q receptor occupancy are incompletely understood. Platelet C1q receptors may contribute to immune complex localization and clearance, as has been suggested for C1q receptors on phagocytic cells (4), but considerable evidence is emerging to suggest that the interaction between C1q and platelets may influence hemostasis and perhaps, more profoundly, thrombotic complications resulting from immune injury. This review will summarize current concepts in C1q receptor biology as it relates to human platelet function and blood coagulation.