Platelets are highly active in shedding their surface molecules. Platelet-associated molecules comprise more than 1,000 proteins: 69 are membrane proteins. Platelets constitutively express molecules that are classically acknowledged to function in primary hemostasis. Clinical observations suggest that thrombocytopenia usually worsens during infection, implying both central and peripheral causes. This review discusses the extended role of platelets as immune cells to emphasize their interactions with infectious pathogens sensed as potentially dangerous.īesides being essential to hemostasis, blood platelets have been recently shown to be able to bind infectious agents or engulf them. Recent findings from in-depth platelet signaling studies reveal the complexity of platelets and some of the ways they evolve along the immune continuum, from beneficial functions exemplified in endothelium repair to deleterious immunopathology as in systemic inflammatory response syndrome and acute vascular diseases. How this occurs is still not fully understood. The sophisticated interplay of platelets with bacteria may culminate in sepsis, a severe pathology characterized by significant reductions in platelet count and platelet dysfunction. This relationship with infectious pathogens may involve other innate immune cells, especially neutrophils. Platelets also express receptors for non-self-infectious and possibly non-infectious danger signals, and can engage infectious pathogens by mechanisms barely explained beyond observation. For example, platelets specialize in pro-inflammatory activities, and can secrete a large number of molecules, many of which display biological response modifier functions. Platelets display a number of properties besides the crucial function of repairing damaged vascular endothelium and stopping bleeding these are exploited to benefit patients receiving platelet component transfusions, which might categorize them as innate immune cells.
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