Related Experiment Video
Updated: Mar 12, 2026
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet-mediated modulation of adaptive immunity
1Division of Immunology, Transplantation and Infectious Diseases, Experimental Imaging Center, IRCCS San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Via Olgettina 58, Milan, 20132, Italy.
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.
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.
Related Concept Videos
01:22Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
01:18Structure and Function of Platelets
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
01:17Intracellular Signaling Affects Focal Adhesions
Some...
01:40Cell-mediated Immune Responses
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
01:24B Cell Activation and Differentiation
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...