Abstract
Hepatic cell populations play an important role during the malaria life cycle. L-SIGN, a homologue of DC-SIGN, mediating leukocyte and pathogen binding, is selectively expressed on liver endothelial cells. Here, we present evidence that L-SIGN acts as an endocytic cell surface receptor. However, P. falciparum-infected erythrocytes did not cytoadhere to L-SIGN. Thus, L-SIGN contributes to elimination of mannosylated ligands but does not participate in hepatic clearance of P. falciparum-infected erythrocytes.
| Original language | English |
|---|---|
| Pages (from-to) | 247-52 |
| Number of pages | 6 |
| Journal | Experimental Parasitology |
| Volume | 96 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Jun 2005 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Animals
- CHO Cells/metabolism
- Cell Adhesion
- Cell Adhesion Molecules/metabolism
- Cricetinae
- Cricetulus
- Erythrocytes/metabolism
- Humans
- Lectins, C-Type/metabolism
- Malaria, Falciparum/metabolism
- Nerve Tissue Proteins/metabolism
- Plasmodium falciparum/physiology
- Receptors, Cell Surface/metabolism
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