ArticleScientific reports2018
Plasmodium falciparum gametocyte-infected erythrocytes do not adhere to human primary erythroblasts.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Erythropoiesis and Malaria, a Multifaceted Interplay.International journal of molecular sciences · 2022Review
- Phagocytosis and activation of bone marrow-derived macrophages by Plasmodium falciparum gametocytes.Malaria journal · 2021Article
- Plasmodium falciparum sexual parasites develop in human erythroblasts and affect erythropoiesis.Blood · 2020Article
- Different distribution of malaria parasite in left and right extremities of vertebrate hosts translates into differences in parasite transmission.Scientific reports · 2020Article
- Plasmodium asexual growth and sexual development in the haematopoietic niche of the host.Nature reviews. Microbiology · 2020Review
- Article
- Revisiting gametocyte biology in malaria parasites.FEMS microbiology reviews · 2019Review
- Erythrocyte Membrane Makeover byFrontiers in microbiology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Plasmodium falciparum gametocytes, the sexual stages responsible for malaria parasite transmission, develop in the human bone marrow parenchyma in proximity to the erythroblastic islands. Yet, mechanisms underlying gametocytes interactions with these islands are unknown. Here, we have investigated whether gametocyte-infected erythrocytes (GIE) adhere to erythroid precursors, and whether a putative adhesion may be mediated by a mechanism similar to the adhesion of erythrocytes infected with P. falciparum asexual stages to uninfected erythrocytes. Cell-cell adhesion assays with human primary erythroblasts or erythroid cell lines revealed that immature GIE do not specifically adhere to erythroid precursors. To determine whether adhesion may be dependent on binding of STEVOR proteins to Glycophorin C on the surface of erythroid cells, we used clonal lines and transgenic parasites that overexpress specific STEVOR proteins known to bind to Glycophorin C in asexual stages. Our results indicate that GIE overexpressing STEVOR do not specifically adhere to erythroblasts, in agreement with our observation that the STEVOR adhesive domain is not exposed at the surface of GIE.
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Registered trials
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