Platelet-mediated modulation of adaptive immunity

Besides being the main cellular effectors of hemostasis, platelets possess a plethora of intracellular mediators (e.g. cytokines, chemokines and antimicrobial molecules) as well as surface receptors (e.g. P-selectin, integrins, CD40L, intercellular adhesion molecule [ICAM]-2, junctional adhesion molecule [JAM]-A, CD44, Toll-like receptors, chemokine receptors) known for their involvement in inflammatory and immune responses. These aspects of platelet biology, which suggest an evolutionary link to a more primitive multifunctional innate defensive cell, position platelets at the interface between coagulation and immunity. Whereas platelet functions in direct antimicrobial defense and in the enhancement of innate immunity are being increasingly recognized, platelet-mediated modulation of adaptive immunity is often underappreciated by the immunological community. By using mouse models of viral hepatitis as a paradigmatic example, we will review here how platelets coordinate adaptive immune responses and suggest possible clinical implications.