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首页> 外文期刊>Virology >Exosome release following activation of the dendritic cell immunoreceptor: A potential role in HIV-1 pathogenesis
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Exosome release following activation of the dendritic cell immunoreceptor: A potential role in HIV-1 pathogenesis

机译:树突状细胞免疫受体激活后外泌体释放:HIV-1发病机制中的潜在作用。

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摘要

Exosomes are extracellular vesicles (EVs) that play a role in intercellular communication. Stimulation of dendritic cells by the HIV-1 virus triggers their release. HIV-1 binds to dendritic cells via dendritic cell immunoreceptor (DCIR). This study shows that inhibiting the binding to DCIR significantly decreases exosome release by HIV-1-pulsed dendritic cells. In addition, exosome release from Raji-CD4 expressing DCIR cells stimulated by anti-DCIR or HIV-1 is decreased when the immunoreceptor tyrosine-based inhibition motif (ITIM) signaling motif of DCIR is mutated. Unlike the EVs released from Raji-CD4-DCIR cells after antibody stimulation, those released from HIV-1-infected cells contain the pro-apoptotic protein DAP-3. Furthermore, EVs from HIV-1 pulsed dendritic cells increase spontaneous apoptosis in uninfected CD4 T lymphocytes while they decrease it in neutrophils. This study describes for the first time that DCIR plays a role in the release of exosomes strengthening the importance of this receptor and EVs/exosomes in HIV-1 pathogenesis. (C) 2015 The Authors. Published by Elsevier Inc.
机译:外泌体是在细胞间通讯中起作用的细胞外囊泡(EV)。 HIV-1病毒刺激树突状细胞触发其释放。 HIV-1通过树突状细胞免疫受体(DCIR)与树突状细胞结合。这项研究表明,抑制与DCIR的结合可显着降低HIV-1脉冲树突状细胞释放外来体。此外,当DCIR的基于免疫受体酪氨酸的抑制基序(ITIM)信号基序发生突变时,由抗DCIR或HIV-1刺激的表达Raji-CD4的DCIR细胞的外泌体释放减少。与抗体刺激后从Raji-CD4-DCIR细胞释放的电动汽车不同,从HIV-1感染的细胞释放的电动汽车含有促凋亡蛋白DAP-3。此外,来自HIV-1脉冲树突状细胞的电动汽车会增加未感染的CD4 T淋巴细胞的自发凋亡,而在嗜中性粒细胞中会降低自发性凋亡。这项研究首次描述了DCIR在释放外泌体中的作用,从而增强了该受体和EVs /外泌体在HIV-1发病机理中的重要性。 (C)2015作者。由Elsevier Inc.发布

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