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Dendritic Cell-Mediated trans-Enhancement of Human Immunodeficiency Virus Type 1 Infectivity Is Independent of DC-SIGN▿

机译:树突状细胞介导的人类免疫缺陷病毒1型感染力的增强与DC-SIGN无关

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摘要

Dendritic cells (DCs) enhance human immunodeficiency virus type 1 (HIV-1) infection of CD4+ T lymphocytes in trans. The C-type lectin DC-SIGN, expressed on DCs, binds to the HIV-1 envelope glycoprotein gp120 and confers upon some cell lines the capacity to enhance trans-infection. Using a short hairpin RNA approach, we demonstrate that DC-SIGN is not required for efficient trans-enhancement by DCs. In addition, the DC-SIGN ligand mannan and an anti-DC-SIGN antibody did not inhibit DC-mediated enhancement. HIV-1 particles were internalized and were protected from protease treatment following binding to DCs, but not from binding to DC-SIGN-expressing Raji cells. Thus, DC-SIGN is not required for DC-mediated trans-enhancement of HIV infectivity.
机译:树突状细胞(DC)增强反式CD4 + T淋巴细胞的人类1型免疫缺陷病毒(HIV-1)感染。在DC上表达的C型凝集素DC-SIGN与HIV-1包膜糖蛋白gp120结合,并赋予某些细胞系增强转染的能力。使用短发夹RNA方法,我们证明DC不需要有效的DC增强DC-SIGN。另外,DC-SIGN配体甘露聚糖和抗DC-SIGN抗体不抑制DC介导的增强。将HIV-1颗粒内在化并与DC结合后免受蛋白酶处理,但不受与表达DC-SIGN的Raji细胞结合的保护。因此,DC介导的HIV感染力转增强不需要DC-SIGN。

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