Editorial: Platelets as Immune Cells in Physiology and Immunopathology.

Abstract

Blood platelets are essential for the earliest stages of coagulation, namely, primary hemostasis. They adhere to damaged vessel endothelium, stick to each other (aggregate), and form clots; this prevents bleeding. For most physicians, those attributes of platelets are exactly what they learned in medical school years ago, and this basic knowledge seems quite enough to allow a valid therapeutic strategy when numbers or hemostatic functions of platelets are aberrant. In some cases, this consists in prescribing anti-platelet drugs (aspirin or more sophisticated drugs) to prevent overly active clotting in cardiovascular and metabolic dysfunctions. In other instances, this consists in prescribing platelet transfusions when the platelet count is dangerously low (or – in exceptional occasions – when platelets are dysfunctional). It could be as simple as that, but in fact, it is often not, because platelets are more versatile than initially thought (or expected) and some modification is needed in many cases (1). To cite only one example, anti-viral treatment of HIV infection causes atheroma and platelet deposition, emphasizing the recently recognized inflammatory function of platelets (2, 3); anti-platelet therapy seems a likely approach, but this is not current practice yet.