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人类免疫缺陷病毒1型通过CC和CXC趋化因子共受体进入纯化的血液树突状细胞。

Human immunodeficiency virus-1 entry into purified blood dendritic cells through CC and CXC chemokine coreceptors.

作者信息

Ayehunie S, Garcia-Zepeda E A, Hoxie J A, Horuk R, Kupper T S, Luster A D, Ruprecht R M

机构信息

Laboratory of Viral Pathogenesis, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.

出版信息

Blood. 1997 Aug 15;90(4):1379-86.

PMID:9269754
Abstract

Blood dendritic cells (DC) are susceptible to both macrophage (M) and T-cell line (T) tropic human immunodeficiency virus type 1. The CC chemokines RANTES, macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, eotaxin, and, to a lesser extent, monocyte chemoattractant protein-1 (MCP-1) and MCP-4 blocked entry of M-tropic virus into blood DC. The CXC chemokine, SDF-1, a fusin (CXCR4 chemokine receptor) ligand, and an antifusin antibody inhibited DC entry by T-tropic virus. Purified blood DC contained CCR1, CCR2, CCR3, and CCR5 as well as the CXCR4 chemokine receptor RNA transcripts and high levels of fusin on the cell surface. The coexpression of multiple chemokine receptors offers a molecular mechanism to explain the permissiveness of DC for both M- and T-tropic viruses.

摘要

血液树突状细胞(DC)对巨噬细胞(M)嗜性和T细胞系(T)嗜性的1型人类免疫缺陷病毒均敏感。CC趋化因子RANTES、巨噬细胞炎性蛋白-1α(MIP-1α)、MIP-1β、嗜酸性粒细胞趋化因子,以及在较小程度上的单核细胞趋化蛋白-1(MCP-1)和MCP-4可阻断M嗜性病毒进入血液DC。CXC趋化因子SDF-1,一种融合素(CXCR4趋化因子受体)配体,以及一种抗融合素抗体可抑制T嗜性病毒进入DC。纯化的血液DC含有CCR1、CCR2、CCR3和CCR5以及CXCR4趋化因子受体RNA转录本,并且细胞表面有高水平的融合素。多种趋化因子受体的共表达提供了一种分子机制,用以解释DC对M嗜性和T嗜性病毒的易感性。

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