DC-SIGN (CD209) mediates dengue virus infection of human dendritic cells

被引：664
作者：
Tassaneetrithep, B
Burgess, TH
Granelli-Piperno, A
Trumpfherer, C
Finke, J
Sun, W
Eller, MA
Pattanapanyasat, K
Sarasombath, S
Birx, DL
Steinman, RM
Schlesinger, S
Marovich, MA
机构：
[1] Walter Reed Army Inst Res, Div Retrovirol, Rockville, MD 20850 USA
[2] Henry M Jackson Fdn Adv Mil Med Dis, Rockville, MD 20850 USA
[3] Naval Med Res Ctr, Dept Virus Dis, Bethesda, MD 20889 USA
[4] Rockefeller Univ, Cellular Physiol & Immunol Lab, New York, NY 10021 USA
[5] Walter Reed Army Inst Res, Dept Virus Dis, Bethesda, MD 20889 USA
[6] Mahidol Univ, Div Instruments Res, Med Siriraj Hosp, Bangkok 10700, Thailand
[7] Mahidol Univ, Dept Immunol, Med Siriraj Hosp, Bangkok 10700, Thailand
来源：
JOURNAL OF EXPERIMENTAL MEDICINE | 2003年 / 197卷 / 07期
关键词：
receptor; flavivirus; lectin; antigen-presenting cells; virus receptor;
D O I：
10.1084/jem.20021840
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Dengue virus is a single-stranded, enveloped RNA virus that productively infects human dendritic cells (DCs) primarily at the immature stage of their differentiation. We now find that all four serotypes of dengue use DC-SIGN (CD209), a C-type lectin, to infect dendritic cells. THP-1 cells become susceptible to dengue infection after transfection of DC-specific ICAM-3 grabbing nonintegrin (DC-SIGN), or its homologue L-SIGN, whereas the infection of dendritic cells is blocked by anti-DC-SIGN antibodies and not by antibodies to other molecules on these cells. Viruses produced by dendritic cells are infections for DC-SIGN- and L-SIGN-bearing THP-1 cells and other permissive cell lines. Therefore, DC-SIGN may be considered as a new target for designing therapies that block dengue infection.
引用
收藏
页码：823 / 829
页数：7
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