Summary
Beyond obvious functions in haemostasis and thrombosis, platelets are considered to
be essential in proinflammatory surroundings such as atherosclerosis, allergy, rheumatoid
arthritis and even cancer. In atherosclerosis, platelets facilitate the recruitment
of inflammatory cells towards the lesion sites and release a plethora of inflammatory
mediators, thereby enriching and boosting the inflammatory milieu. Platelets do so
by interacting with endothelial cells, circulating leukocytes (monocytes, neutrophils,
dendritic cells, T-cells) and progenitor cells. This cross-talk enforces leukocyte
activation, adhesion and transmigration. Furthermore, platelets are known to function
in innate host defense through the release of antimicrobial peptides and the expression
of pattern recognition receptors. In severe sepsis, platelets are able to trigger
the formation of neutrophil extracellular traps (NETs), which bind and clear pathogens.
The present antiplatelet therapies that target key pathways of platelet activation
and aggregation therefore hold the potential to modulate platelet-derived immune functions
by reducing cellular interactions of platelets with other immune components and by
reducing the secretion of inflammatory proteins into the milieu. The objective of
this review is to update and discuss the current perceptions of the platelet immune
constituents and their prospect as therapeutic targets in an atherosclerotic setting.
Keywords
Inflammation - atherosclerosis - platelet immunology