Accessible cholesterol levels in human red blood cells were found to be stable within individuals but vary >10-fold among individuals and this variability may contribute to differences in cholesterol trafficking among tissues.
Red blood cells infected by the malaria parasite Plasmodium falciparum are destroyed by human natural killer cells in the presence of antibodies from people who have acquired clinical immunity to malaria.
Transcription profiling of activated cells using Phospho-Trap, a new method for identifying activated cells, reveals a critical role for mTOR signaling in red blood cell development and the pathogenesis of anemia
Plasmodium falciparum invasion protein EBA-175, once shed from the parasite surface post invasion, facilitates RBC clustering and enhances parasite growth while simultaneously enabling parasite immune evasion of host neutralizing antibodies.
The bond-based adhesion model is a key step toward a realistic description of RBC-parasite interaction, which allows the investigation of more realistic scenarios and is relevant for other biological systems.