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Lipocalin 2 bolsters innate and adaptive immune responses to blood-stage malaria infection by reinforcing host iron metabolism. (Cevayir COBAN in Cell Host & Microbe)
Plasmodium parasites multiply within host erythrocytes, which contain high levels of iron, and parasite egress from these cells results in iron release and host anemia. Although Plasmodium requires host iron for replication, how host iron homeostasis and responses to these fluxes affect Plasmodium infection are incompletely understood.
The authors determined that Lipocalin 2, a host protein that sequesters iron, is abundantly secreted during human (P. vivax) and mouse (P. yoeliiNL) blood-stage malaria infections and is essential to control P. yoeliiNL parasitemia, anemia, and host survival. During infection, Lcn2 bolsters both host macrophage function and granulocyte recruitment and limits reticulocytosis, or the expansion of immature erythrocytes, which are the preferred target cell of P. yoeliiNL. They further demonstrate that a chronic iron imbalance due to a Lipocalin 2 deficiency results in impaired adaptive immune responses against Plasmodium. Thus, Lipocalin 2 exerts antiparasitic effects by maintaining iron homeostatis and promoting innate and adaptive immune responses. In summary, Lipocalin 2 has multiple tasks in immunity against malaria.
Immunology Frontier Research Center (WPI-IFReC), Osaka University