ArticleBlood advances2022
Malaria-associated adhesion molecule activation facilitates the destruction of uninfected red blood cells.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Innate immune sensing of Plasmodium sporozoite cell traversal drives protective T cell responses.Nature microbiology · 2026Article
- Blood group antigens and malaria susceptibility.Frontiers in cellular and infection microbiology · 2025Review
- The Role of Lutheran/Basal Cell Adhesion Molecule in Hematological Diseases and Tumors.International journal of molecular sciences · 2024Review
- Retention of uninfected red blood cells causing congestive splenomegaly is the major mechanism of anemia in malaria.American journal of hematology · 2024Article
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12 authors.
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Abstract
Severe malarial anemia (SMA) is the main cause of malaria-associated infant mortality in malaria endemic countries. One major factor that contributes to SMA is the accumulation of uninfected red blood cells (uRBCs) in the spleen. We report the activation of adhesion molecules Lutheran/basal cell adhesion molecule (Lu/BCAM) and CD44 on uRBCs from Plasmodium falciparum in vitro cultures and patients with malaria that mediates adherence to the splenic extracellular matrix (ECM) components laminin-α5 and hyaluronic acid (HA), respectively. This tight ECM-adhesion molecule interaction was associated with elevated intracellular Ca2+ levels, increased shedding of microvesicles, and Lu/BCAM clustering on altered uRBCs. Moreover, we observed that a soluble parasite-derived factor promoted the adhesive phenotype of uRBCs, as the incubation of RBCs with filtered malaria-conditioned medium reproduced the same adhesive effect in malaria culture-derived uRBCs. Eventually, Lu/BCAM and CD44 activation facilitate the adherence to ECM components of the red pulp, resulting in the enhanced splenic retention of uRBCs. Our results suggest a novel adhesion molecule-dependent mechanism that augments malaria-induced anemia.
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