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Platelet Interaction with Innate Immune Cells
#MMPMID27226790
Kral JB
; Schrottmaier WC
; Salzmann M
; Assinger A
Transfus Med Hemother
2016[Mar]; 43
(2
): 78-88
PMID27226790
show ga
Beyond their traditional role in haemostasis and thrombosis, platelets are
increasingly recognised as immune modulatory cells. Activated platelets and
platelet-derived microparticles can bind to leukocytes, which stimulates mutual
activation and results in rapid, local release of platelet-derived cytokines.
Thereby platelets modulate leukocyte effector functions and contribute to
inflammatory and immune responses to injury or infection. Platelets enhance
leukocyte extravasation, differentiation and cytokine release.
Platelet-neutrophil interactions boost oxidative burst, neutrophil extracellular
trap formation and phagocytosis and play an important role in host defence.
Platelet interactions with monocytes propagate their differentiation into
macrophages, modulate cytokine release and attenuate macrophage functions.
Depending on the underlying pathology, platelets can enhance or diminish
leukocyte cytokine production, indicating that platelet-leukocyte interactions
represent a fine balanced system to restrict excessive inflammation during
infection. In atherosclerosis, platelet interaction with neutrophils, monocytes
and dendritic cells accelerates key steps of atherogenesis by promoting leukocyte
extravasation and foam cell formation. Platelet-leukocyte interactions at sites
of atherosclerotic lesions destabilise atherosclerotic plaques and promote plaque
rupture. Leukocytes in turn also modulate platelet function and production, which
either results in enhanced platelet destruction or increased platelet production.
This review aims to summarise the key effects of platelet-leukocyte interactions
in inflammation, infection and atherosclerosis.
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