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Glycosylphosphatidylinositol (GPI) anchor of  Plasmodium falciparum  origin is considered an important toxin leading to severe malaria pathology through stimulation of pro-inflammatory responses from innate immune cells. Even though the GPI-induced immune response is widely described to be mediated by pattern recognition receptors such as TLR2 and TLR4, previous studies have revealed that these two receptors are dispensable for the development of severe malaria pathology. Therefore, this study aimed at the identification of potential alternative  Plasmodium  GPI receptors. Herein, we have identified the host protein moesin as an interaction partner of  Plasmodium  GPI  in vitro . Given previous reports indicating the relevance of moesin especially in the LPS-mediated induction of pro-inflammatory responses, we have conducted a series of  in vitro  and  in vivo  experiments to address the physiological relevance of the moesin- Plasmodium  GPI interaction in the context of malaria pathology. We report here that although moesin and  Plasmodium  GPI interact  in vitro , moesin is not critically involved in processes leading to  Plasmodium -induced pro-inflammatory immune responses or malaria-associated cerebral pathology.

Interaction between Plasmodium Glycosylphosphatidylinositol and the Host Protein Moesin Has No Implication in Malaria Pathology