Platelets and innate immunity

Abstract

Although platelets are best known as primary mediators of hemostasis, this function intimately associates them with inflammatory processes, and it has been increasingly recognized that platelets play an active role in both innate and adaptive immunity. For example, platelet adhesive interactions with leukocytes and endothelial cells via P-selectin can lead to several pro-inflammatory events, including leukocyte rolling and activation, production of cytokine cascades, and recruitment of the leukocytes to sites of tissue damage. Superimposed on this, platelets express immunologically-related molecules such as CD40L and Toll-like receptors that have been shown to functionally modulate innate immunity. Furthermore, platelets themselves can interact with microorganisms, and several viruses have been shown to cross-react immunologically with platelet antigens. This review discusses the central role that platelets play in inflammation, linking them with varied pathological conditions, such as atherosclerosis, sepsis, and immune thrombocytopenic purpura, and suggests that platelets also act as primary mediators of our innate defences.

Fig. 1

Linking platelets to immunity by phenotype. Platelets store/express and secrete many immunomodulatory molecules and that can significantly affect innate immune mechanisms. Some are constitutively expressed whiles others are expressed or secreted upon platelet activation while still others are acquired by either adsorption from the plasma or perhaps by platelet contact with activated leukocytes during inflammation and subsequent membrane redistribution. Also included are MHC class I molecules and the two major platelet-specific glycoproteins, CD41 and CD42, to indicate the major antigenic proteins recognized by host adaptive immunity