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. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: Shock. 2021 Feb 1;55(2):156–166. doi: 10.1097/SHK.0000000000001619

Fig. 2. Platelet–monocyte interactions.

Fig. 2.

A, Activated platelets upregulate surface expression of P-selectin, which binds to receptor P-selectin glycoprotein ligand-1 (PSGL-1). This initiates aggregation of platelets and monocytes. Aggregation is further consolidated by potentiation of other ligand–receptor interactions, including CD40L (CD154) with CD11b/CD18 (MAC-1). Simultaneously, activated platelets release chemokines and cytokines (e.g., PF4, RANTES, TGFβ), which bind to cognate receptors on monocytes, initiating intracellular signal transduction and alteration of monocyte function. B, Monocytes are activated after aggregation with platelets, and release a variety of proinflammatory cytokines (e.g., IL6, IL1β, TNFα), which contribute to the dysregulated inflammatory response after sepsis. C, Aggregation of platelets and monocytes induces expression of adherent molecules on monocyte cell surface and promotes monocyte–endothelial interactions and potentiates monocyte transmigration to the infection site. D, Platelets–monocyte aggregation induces M1 polarization of monocytes.