Different PfEMP1-expressing Plasmodium falciparum variants induce divergent endothelial transcriptional responses during cytoadherence

ABSTRACT: The pathogenesis of severe malaria is complex and involves several pathways that influence host inflammation and endothelial function. The human malaria parasite Plasmodium falciparum is responsible for the majority of mortality and morbidity caused by malaria infection and differs from other human malaria species in the degree of accumulation of parasite-infected red blood cells in the microvasculature, known as cytoadherence or sequestration. In P. falciparum, cytoadherence is mediated by a protein called PfEMP1 which, due to its exposure to the host immune system, undergoes antigenic variation resulting in the expression of different PfEMP1 variants on the infected erythrocyte membrane. These PfEMP1s contain various combinations of adhesive domains, which allow for the differential e

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER: Leo Zeef 

PROVIDER: E-MTAB-12730 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress