Figure 3.

Anemia, HO‐1, and IL‐10. During malaria infection, anemia can occur through direct lysis of parasitized RBCs (hemolysis) or through eryptosis of uninfected RBCs—which are taken up by phagocytes through the phosphatidylserine receptor (PSR). Hemolysis results in release of hemoglobin (Hb), which can be further degraded to free heme. Serum scavenger proteins haptoglobin (Hpt) and hemopexin (Hpx) bind Hb and heme before uptake by phagocytes through CD163 and CD91, respectively. Intracellular heme is then degraded to iron, biliverdin, and carbon monoxide via the enzyme HO‐2 or the inducible isoform, HO‐1. HO‐1 can also be induced by IL‐10 receptor signaling. The impact of IL‐10 and HO‐1 during malarial anemia and hemolysis on phagocyte function remains poorly defined