Platelets: killers of parasites or patients?

In this issue of Blood, Gramaglia et al have provided valuable data on whether platelets are protective in malaria infection by directly killing Plasmodium parasites, or deleterious by driving adverse immune responses. Platelets are the cellular mediators of thrombosis. Although this is a very important biologic role, platelets are also the most numerous circulating cell with an inflammatory and immune modulatory function. The first, and still the best understood, disease context for platelet-driven inflammation is atherosclerosis. More recently, platelets have been shown to have important, largely adverse roles, in infectious disease processes such as sepsis, bacterial infections, viral infections, and parasitic infections, including infections with the malaria causative agent Plasmodium. With an increased appreciation for the immune and inflammatory functions of platelets in many diseases, there have been an increased number of studies, including study into platelets in malaria infection. There have been conflicting conclusions on whether platelets are “good or bad” players in malaria infection. Although there is a broad sense that platelets are proinflammatory and initiate or accelerate immune cell responses to infection in general, some reports have indicated a potential direct antiPlasmodium parasite-killing role for platelets (see figure). This paper by Gramaglia et al provides a further understanding of whether platelets directly kill Plasmodium parasites, and if they do, does it actually limit the in vivo parasite burden.