Pluripotent Stem Cell-Derived Hepatocytes Inhibit T Cell Proliferation In Vitro through Tryptophan Starvation.
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Authors
Elgueta, Raul
McCluskey, Daniel
Stolarczyk, Emilie
Lucendo-Villarin, Baltasar
Meseguer-Ripolles, Jose
Fanelli, Giorgia
Watt, Fiona M
Lombardi, Giovanna
Publication Date
2021-12-22Journal Title
Cells
ISSN
2073-4409
Publisher
MDPI AG
Volume
11
Issue
1
Language
eng
Type
Article
This Version
VoR
Metadata
Show full item recordCitation
Romano, M., Elgueta, R., McCluskey, D., Ortega-Prieto, A. M., Stolarczyk, E., Dazzi, F., Lucendo-Villarin, B., et al. (2021). Pluripotent Stem Cell-Derived Hepatocytes Inhibit T Cell Proliferation In Vitro through Tryptophan Starvation.. Cells, 11 (1) https://doi.org/10.3390/cells11010024
Abstract
Regenerative medicine aims to replace damaged tissues by stimulating endogenous tissue repair or by transplanting autologous or allogeneic cells. Due to their capacity to produce unlimited numbers of cells of a given cell type, pluripotent stem cells, whether of embryonic origin or induced via the reprogramming of somatic cells, are of considerable therapeutic interest in the regenerative medicine field. However, regardless of the cell type, host immune responses present a barrier to success. The aim of this study was to investigate in vitro the immunological properties of human pluripotent stem cell (PSC)-derived hepatocyte-like cells (HLCs). These cells expressed MHC class I molecules while they lacked MHC class II and co-stimulatory molecules, such as CD80 and CD86. Following stimulation with IFN-γ, HLCs upregulated CD40, PD-L1 and MHC class I molecules. When co-cultured with allogeneic T cells, HLCs did not induce T cell proliferation; furthermore, when T cells were stimulated via αCD3/CD28 beads, HLCs inhibited their proliferation via IDO1 and tryptophan deprivation. These results demonstrate that PSC-derived HLCs possess immunoregulatory functions, at least in vitro.
Keywords
T cell activation, in vitro studies, Regenerative Medicine, Ipsc-derived Hepatocyte-like Cells
Sponsorship
Medical Research Council (MR/L022699/1, MR/S020934/1)
Chief Scientist Office (TCS 16/37)
Identifiers
35011586, PMC8750013
External DOI: https://doi.org/10.3390/cells11010024
This record's URL: https://www.repository.cam.ac.uk/handle/1810/333893
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