The impact of platelets and antiplatelets medications on immune mediation

Abstract

Objective: To investigate the mechanisms through which platelets and antiplatelet therapies modulate the immune response and propose directions for future research in this field, with a particular emphasis on their impact on treatment efficacy and surgical outcomes.

Methods: A comprehensive review of recent studies investigating the role of platelets in immune modulation, specifically highlighting their involvement in pathogen recognition, leukocyte recruitment, and lymphocyte activation. Additionally, the review evaluates the impact of antiplatelet therapies, such as aspirin, P2Y12 inhibitors, and glycoprotein IIb/IIIa inhibitors, on immune responses.

Results: Recent studies have emphasized the critical role of platelets in immune-driven applications, namely, atherosclerosis, cancer, viral infections, and sepsis. These studies also suggest that antiplatelet therapies may alter immune responses. However, the precise mechanisms through which platelets and antiplatelet drugs influence immune responses, as well as their effects on post-treatment and surgical outcomes, are not yet fully elucidated.

Conclusions: Recent studies highlight the important role of platelets in immune processes, such as in atherosclerosis, cancer, viral infections, and sepsis, and suggest that antiplatelet therapies can influence immune responses. However, the exact mechanisms by which platelets and antiplatelet drugs modulate these responses remain unclear. This area presents valuable opportunities for future research to uncover these mechanisms, which could lead to novel therapeutic strategies and better clinical outcomes for patients.

Keywords: Antiplatelets; Immune response; Immunology; Platelets.

Fig

Modulatory mechanisms carried out by activated platelets in the body's innate and adaptive immune responses, showing (A) the role of platelets in the formation of platelet-neutrophil aggregate (PNA) and in the production of neutrophils extracellular traps (NETs) as well as in the formation of platelet-monocyte aggregation (PMA) and innate immune cell adhesion on the endothelial wall. (B) Tumor evasion promoted by platelets through the stimulation of fibrinogen production by fibroblasts, reducing the exposure of tumor major histocompatibility complex (MHC) I molecules. (C) The role of platelets in redirecting pathogenic antigens to CD8α⁺ dendritic cells (DCs) and in promoting cytotoxic CD8⁺ T cell effector mechanisms against cells infected with intracellular pathogens and (D) role of platelets in isotype switching and antibody production by B cells activated through CD40-CD40L signaling.