期刊
TRAFFIC
卷 18, 期 4, 页码 218-231出版社
WILEY
DOI: 10.1111/tra.12469
关键词
antigen-presenting cells; C-type lectin receptor; DC-SIGN; dengue virus; fluorescence microscopy; in vivo trafficking; quantitative colocalization; super-resolution imaging; viral entry; viral receptor
类别
资金
- NIH [R01-GM041402, T32-CA009156, RO1-AI107731]
- North Carolina Biotechnology Center Institutional Support [2012-IDG-1006]
- NIH Cancer Center Core [P30 CA016086]
Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), a C-type lectin expressed on the plasma membrane by human immature dendritic cells, is a receptor for numerous viruses including Ebola, SARS and dengue. A controversial question has been whether DC-SIGN functions as a complete receptor for both binding and internalization of dengue virus (DENV) or whether it is solely a cell surface attachment factor, requiring either hand-off to another receptor or a co-receptor for internalization. To examine this question, we used 4 cell types: human immature dendritic cells and NIH3T3 cells expressing either wild-type DC-SIGN or 2 internalization-deficient DC-SIGN mutants, in which either the 3 cytoplasmic internalization motifs are silenced by alanine substitutions or the cytoplasmic region is truncated. Using confocal and super-resolution imaging and high content single particle tracking, we investigated DENV binding, DC-SIGN surface transport, endocytosis, as well as cell infectivity. DC-SIGN was found colocalized with DENV inside cells suggesting hand-off at the plasma membrane to another receptor did not occur. Moreover, all 3 DC-SIGN molecules on NIH3T3 cells supported cell infection. These results imply the involvement of a co-receptor because cells expressing the internalization-deficient mutants could still be infected.
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