The interaction between DC and Plasmodium berghei/chabaudi-infected erythrocytes in mice involves direct cell-to-cell contact, internalization and TLR.

Early interactions between blood-stage Plasmodium parasites and cells of the innate immune system are very important in shaping the adaptive immune response to malaria, and a number of studies have suggested that DC are responsible for this phenomenon. Therefore, we examined the capacity of murine BM-derived DC to internalize parasites, be activated and produce cytokines upon in vitro interaction with murine erythrocytes infected with two different strains of rodent malaria parasites (Plasmodium berghei and Plasmodium chabaudi chabaudi). We show that the increased expression of MHC class II and co-stimulatory molecules and increased production of cytokines by DC following Plasmodium infection involves internalization of infected RBC. Such DC activation not only requires direct cell-to-cell contact and internalization of infected RBC by DC but also involves TLR4, TLR9, MyD88 and signaling via NF-kappaB; however, TLR involvement in survival to Plasmodium infection was found to be negligible.