Platelets have been extensively studied in the context of coagulation and their hemostatic imbalance can lead to conditions as atherosclerotic plaques and thrombosis. Nevertheless, the knowledge regarding the regulation of immune cell types by platelets has been growing exponentially in the past years. Among these biological systems, the innate immunity is remarkably affected by the crosstalk with platelets. This interaction comes from the formation of platelet-leukocyte aggregates, signaling by direct contact or by stimulation of immune cells by soluble factors and microparticles secreted by platelets. These blood components can sense and react danger signals, guiding leukocytes to injury sites and providing a scaffold for the formation of extracellular traps for microbial clearance. Using different mechanisms, platelets have the task to regulate the release of cytokines and chemokines upon sterile or infectious damage, modulate the expression of cell markers and control cell death and survival. Therefore, platelets are more than clotting agents, but critical players within the immune equilibrium for the host. Here we present an understanding about how platelets modulate innate immune cells, as well as a summary of the outcome of this interaction, an important step for therapeutic opportunities and future research on infectious and autoimmune diseases.
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Institute of Innate Immunity
