Cytochalasin B-Induced Membrane Vesicles from Human Mesenchymal Stem Cells Overexpressing IL2 Are Able to Stimulate CD8
cancer therapy
cytochalasin B
extracellular vesicles
human triple negative breast cancer
immune cell activation
immunotherapy
interleukin 2
mesenchymal stem cells
Journal
Biology
ISSN: 2079-7737
Titre abrégé: Biology (Basel)
Pays: Switzerland
ID NLM: 101587988
Informations de publication
Date de publication:
10 Feb 2021
10 Feb 2021
Historique:
received:
14
12
2020
revised:
05
02
2021
accepted:
06
02
2021
entrez:
13
2
2021
pubmed:
14
2
2021
medline:
14
2
2021
Statut:
epublish
Résumé
Interleukin 2 (IL2) was one of the first cytokines used for cancer treatment due to its ability to stimulate anti-cancer immunity. However, recombinant IL2-based therapy is associated with high systemic toxicity and activation of regulatory T-cells, which are associated with the pro-tumor immune response. One of the current trends for the delivery of anticancer agents is the use of extracellular vesicles (EVs), which can carry and transfer biologically active cargos into cells. The use of EVs can increase the efficacy of IL2-based anti-tumor therapy whilst reducing systemic toxicity. In this study, human adipose tissue-derived mesenchymal stem cells (hADSCs) were transduced with lentivirus encoding IL2 (hADSCs-IL2). Membrane vesicles were isolated from hADSCs-IL2 using cytochalasin B (CIMVs-IL2). The effect of hADSCs-IL2 and CIMVs-IL2 on the activation and proliferation of human peripheral blood mononuclear cells (PBMCs) as well as the cytotoxicity of activated PBMCs against human triple negative cancer MDA-MB-231 and MDA-MB-436 cells were evaluated. The effect of CIMVs-IL2 on murine PBMCs was also evaluated in vivo. CIMVs-IL2 failed to suppress the proliferation of human PBMCs as opposed to hADSCs-IL2. However, CIMVs-IL2 were able to activate human CD8
Identifiants
pubmed: 33579033
pii: biology10020141
doi: 10.3390/biology10020141
pmc: PMC7916789
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Russian Science Foundation
ID : 18-74-10044
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