Platelets and innate immunity |
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Authors: | John W Semple John Freedman |
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Institution: | (1) Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, 30 Bond Street, Toronto, ON, M5B 1W8, Canada;(2) Department of Pharmacology, University of Toronto, Toronto, ON, Canada;(3) Department of Medicine, University of Toronto, Toronto, ON, Canada;(4) Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada;(5) Canadian Blood Services, Toronto, ON, Canada;(6) The Toronto Platelet Immunobiology Group, Toronto, ON, Canada |
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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. |
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