Plateletleukocyte

Plateletleukocyte, or platelet-leukocyte interaction, refers to the physical and functional contacts between platelets and leukocytes that lead to the formation of platelet-leukocyte aggregates (PLA). These interactions are a component of thromboinflammation, linking hemostasis and innate immunity.

Formation and mechanisms of interaction begin when platelets are activated, causing the surface expression of P-selectin. P-selectin binds to P-selectin glycoprotein ligand-1 on neutrophils and monocytes, promoting adhesion. Additional interactions involve platelet-derived CD40L binding to CD40 on leukocytes, as well as bridging by von Willebrand factor via GPIb-IX-V and chemokines released by activated platelets that recruit leukocytes. These mechanisms enable direct cell-to-cell contact and signaling between platelets and various leukocyte subsets.

PLA contribute to leukocyte recruitment, amplified inflammatory responses, and the formation of neutrophil extracellular traps, while also potentially promoting leukocyte activation and transmigration across the endothelium. They can influence thrombus growth and stability in inflamed vessels, representing a link between inflammatory and thrombotic processes.

Clinical relevance and detection often focus on increased PLA in conditions such as acute coronary syndromes, atherosclerosis, diabetes, and sepsis, where higher PLA levels have been associated with adverse outcomes in some studies. Detection is typically performed by flow cytometry on peripheral blood, identifying platelets bound to leukocytes (for example, CD41/CD61 marking platelets and CD45+ marking leukocytes, with further subdivisions like CD14+ monocytes or CD15+ neutrophils).

Therapeutically, PLA formation depends on platelet activation, so antiplatelet therapies can reduce their occurrence. Ongoing research examines PLA as biomarkers of thromboinflammation and as targets for intervention.