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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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CHO Cells / metabolism
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CHO Cells / parasitology*
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Cell Adhesion
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Cell Adhesion Molecules / metabolism*
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Cricetinae
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Cricetulus
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Erythrocytes / metabolism
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Erythrocytes / parasitology*
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Humans
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Lectins, C-Type / metabolism*
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Malaria, Falciparum / metabolism
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Malaria, Falciparum / parasitology*
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Nerve Tissue Proteins / metabolism*
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Plasmodium falciparum / physiology*
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Receptors, Cell Surface / metabolism*
Substances
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CLEC4M protein, human
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Cell Adhesion Molecules
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Lectins, C-Type
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Nerve Tissue Proteins
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Receptors, Cell Surface