期刊
EMBO JOURNAL
卷 40, 期 8, 页码 -出版社
WILEY
DOI: 10.15252/embj.2020105492
关键词
exosomes; extracellular vesicles; HIV; proteomics; T cells
资金
- INSERM
- Institut Curie
- NIDA [DA040385, DA047807]
- ANRS [2015-1 CT]
- SIDACTION [17-1-AAE-1138]
- INCa [INCA-11548]
- Fondation ARC [PGA1 RF20180206962]
- French National Research Agency [ANR-10-IDEX-0001-02 PSL*, ANR-11-LABX-0043, ANR-18-CE13-0017-03]
- NIH Common Fund through the Office of Strategic Coordination/Office of the NIH Director [UG3CA241694]
- Region Ile-de-France
- Fondation pour la Recherche Medicale
- French National Research Agency through the Investments for the Future program (France-BioImaging) [ANR-10-INSB-04]
- CelTisPhyBio Labex part of the IDEX PSL [ANR-10-LBX-0038, ANR-10-IDEX-0001-02 PSL]
- Max Planck Society for the Advancement of Science
- German Research Foundation (DFG) [MA 1764/2-1]
This study developed a proteomic profiling approach to study EV subtype composition and identified changes in cellular protein profiles in EVs upon HIV infection. The research also found that SERINC3 plays a role in controlling the surface composition of EVs.
Cells release diverse types of extracellular vesicles (EVs), which transfer complex signals to surrounding cells. Specific markers to distinguish different EVs (e.g. exosomes, ectosomes, enveloped viruses like HIV) are still lacking. We have developed a proteomic profiling approach for characterizing EV subtype composition and applied it to human Jurkat T cells. We generated an interactive database to define groups of proteins with similar profiles, suggesting release in similar EVs. Biochemical validation confirmed the presence of preferred partners of commonly used exosome markers in EVs: CD81/ADAM10/ITGB1, and CD63/syntenin. We then compared EVs from control and HIV-1-infected cells. HIV infection altered EV profiles of several cellular proteins, including MOV10 and SPN, which became incorporated into HIV virions, and SERINC3, which was re-routed to non-viral EVs in a Nef-dependent manner. Furthermore, we found that SERINC3 controls the surface composition of EVs. Our workflow provides an unbiased approach for identifying candidate markers and potential regulators of EV subtypes. It can be widely applied to in vitro experimental systems for investigating physiological or pathological modifications of EV release.
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