Results published in Cell suggest two molecular mechanisms whereby sickle Hb confers host tolerance to severe forms of malaria. First, the sickle cell mutations act via strongly inducing heme oxygenase-1 (HO-1). Ho-1 produces carbon monoxide which confers protection against cerebral malaria (Cell. 2011 Apr 29;145(3):398-409). CO blocks accumulation of circulating free heme after Plasmodium infection, suppressing pathogenesis. Second, sickle Hb inhibits activation pathogenic CD8(+) T cells that recognize Plasmodium antigens, as an immunoregulatory effect.
Results published in Cell suggest two molecular mechanisms whereby sickle Hb confers host tolerance to severe forms of malaria. First, the sickle cell mutations act via strongly inducing heme oxygenase-1 (HO-1). Ho-1 produces carbon monoxide which confers protection against cerebral malaria (Cell. 2011 Apr 29;145(3):398-409). CO blocks accumulation of circulating free heme after Plasmodium infection, suppressing pathogenesis. Second, sickle Hb inhibits activation pathogenic CD8(+) T cells that recognize Plasmodium antigens, as an immunoregulatory effect.