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We found that CD44 can be efficiently deleted from primary human hematopoietic stem cells using CRISPR\/Cas9 genome editing, and that the efficiency of ex\u00a0vivo erythropoiesis to enucleated cultured red blood cells (cRBCs) is not affected by lack of CD44. However, the rate of P falciparum invasion was reduced in CD44-null cRBCs relative to isogenic wild-type control cells, validating CD44 as an important host factor for this parasite. We identified 2 P falciparum invasion ligands as binding partners for CD44, erythrocyte binding antigen 175 (EBA-175) and EBA-140 and demonstrated that their ability to bind to human erythrocytes relies primarily on their canonical receptors, glycophorin A and glycophorin C, respectively. We further show that EBA-175 induces phosphorylation of erythrocyte cytoskeletal proteins in a CD44-dependent manner. Our findings support a model in which P falciparum exploits CD44 as a coreceptor during invasion of human erythrocytes, stimulating CD44-dependent phosphorylation of host cytoskeletal proteins that alter host cell deformability and facilitate parasite entry.<\/jats:p>","DOI":"10.1182\/blood.2023020831","type":"journal-article","created":{"date-parts":[[2023,10,13]],"date-time":"2023-10-13T20:11:20Z","timestamp":1697227880000},"page":"2016-2028","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":16,"title":["<i>Plasmodium falciparum<\/i> exploits CD44 as a coreceptor for erythrocyte invasion"],"prefix":"10.1182","volume":"142","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7780-1744","authenticated-orcid":false,"given":"Barbara","family":"Baro","sequence":"first","affiliation":[{"name":"1Department of Pediatrics, Stanford University School of Medicine, Stanford, 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