Table 1.

Summary of studies of molecules associated with platelet-monocyte aggregate formation

Species	Ex vivo/in vivo	PMA detection method	Involved molecules	Main findings
Human	Ex vivo	Light microscopy and flowcytometry	GPIIb-IIIa on platelets	GPIIb-IIIa on platelets had a supportive role in the formation of PMA only in the presence of weak activation of platelets (50)
Human	Ex vivo	Flowcytometry	GPIIb-IIIa on platelets	GPIIb-IIIa antagonist inhibited the formation of PMA and monocyte tissue factor expression after platelets activation (51)
Mouse	Ex vivo	Flowcytometry	ICAM-1 on monocytes	ICAM-1 on monocytes bound to the fibrinogen attached to the activated platelets as to facilitate the formation of PMA (46)
Human and mouse	Ex vivo and in vivo	Flowcytometry	Monocyte EMMPRIN (CD147/basigin) and platelet GPVI	EMMPRIN-GPVI engagement facilitated formation of PMA in vivo and ex vivo (47)
Human	Ex vivo	Flowcytometry	Platelet P-selectin (CD62P) and monocyte PSGL-1	CD62P-PSGL-1 engagement was responsible for formation of PMA (13)
Human	Ex vivo	Flowcytometry	Platelet P-selectin (CD62P)	Platelet activation (increased expression of CD62P) was, not monocyte activation, led to increased formation of PMA (45)
Human	Ex vivo	Flowcytometry	Platelet P-selectin (CD62P) and monocyte PSGL-1	P-selectin-PSGL-1 engagement induced monocyte activation via upregulation of IL1β and TNFα by NF-κB translocation into nucleus (60)
Human	Ex vivo	Flowcytometry	Platelet P-selectin (CD62P) and monocyte PSGL-1	P-selectin-PSGL-1 engagement induced monocyte upregulation of IL8 and tissue factor by phosphorylation of Lyn, which could be inhibited by IL10 (65)
Human	Ex vivo	Flowcytometry	Platelet P-selectin (CD62P) and Phosphatidylserine	P-selectin-mediated binding and Phosphatidylserine recognition on activated platelets induced monocyte secretion of IL8 and IL10 (53)