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Cell ; 173(2): 443-455.e12, 2018 04 05.
Article in English | MEDLINE | ID: mdl-29576450

ABSTRACT

Hereditary xerocytosis is thought to be a rare genetic condition characterized by red blood cell (RBC) dehydration with mild hemolysis. RBC dehydration is linked to reduced Plasmodium infection in vitro; however, the role of RBC dehydration in protection against malaria in vivo is unknown. Most cases of hereditary xerocytosis are associated with gain-of-function mutations in PIEZO1, a mechanically activated ion channel. We engineered a mouse model of hereditary xerocytosis and show that Plasmodium infection fails to cause experimental cerebral malaria in these mice due to the action of Piezo1 in RBCs and in T cells. Remarkably, we identified a novel human gain-of-function PIEZO1 allele, E756del, present in a third of the African population. RBCs from individuals carrying this allele are dehydrated and display reduced Plasmodium infection in vitro. The existence of a gain-of-function PIEZO1 at such high frequencies is surprising and suggests an association with malaria resistance.


Subject(s)
Anemia, Hemolytic, Congenital/pathology , Black People/genetics , Hydrops Fetalis/pathology , Ion Channels/genetics , Malaria/pathology , Alleles , Anemia, Hemolytic, Congenital/genetics , Animals , Dehydration , Disease Models, Animal , Erythrocytes/cytology , Erythrocytes/metabolism , Gene Deletion , Genotype , Humans , Hydrops Fetalis/genetics , Intermediate-Conductance Calcium-Activated Potassium Channels/deficiency , Intermediate-Conductance Calcium-Activated Potassium Channels/genetics , Ion Channels/chemistry , Malaria/genetics , Malaria/parasitology , Malaria/prevention & control , Mice , Mice, Inbred C57BL , Mice, Knockout , Phenotype , Plasmodium berghei/growth & development , Plasmodium berghei/pathogenicity , T-Lymphocytes/cytology , T-Lymphocytes/metabolism
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