Exosome release following activation of the dendritic cell immunoreceptor: A potential role in HIV-1 pathogenesis

被引：20

作者：

Mfunyi, Claude M. ^{[1
]}

Vaillancourt, Myriam ^{[1
]}

Vitry, Julien ^{[1
]}

Batomene, Thy-Rene Nsimba ^{[1
]}

Posvandzic, Alma ^{[1
]}

Lambert, Alexandra A. ^{[1
]}

Gilbert, Caroline ^{[1
]}

机构：

[1] Univ Laval, Fac Med, Dept Microbiol Infectiol Immunol, Ctr Rech,CHU Quebec, Quebec City, PQ G1K 7P4, Canada

来源：

VIROLOGY | 2015年 / 484卷

基金：

加拿大健康研究院;

关键词：

AIDS; Apoptosis; DCIR; Dendritic cells; Extracellular vesicles; Exosomes; HIV-1; CD4 T lymphocytes; Neutrophils; HUMAN-IMMUNODEFICIENCY-VIRUS; CD4(+) T-CELLS; INFECTION; NEUTROPHILS; EXPRESSION; RESPONSES; CLECSF6; TYPE-1; ITIM;

D O I：

10.1016/j.virol.2015.05.013

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

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.

引用

页码：103 / 112

页数：10

共 36 条

[1]

Caroline Subra, 2011, EXOSOMES DECREASE IN

[2] The C-type lectin surface receptor DICIR acts as a new attachment factor for HIV-1 in dendritic cells and contributes to trans- and cis-infection pathways [J].