Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation

Abstract Acute graft-versus-host disease (GVHD) is characterized by severe tissue damage that is a life-threatening complication of allogeneic hematopoietic stem cell transplantation. Due to their immunosuppressive properties, mesenchymal stem cells (MSC) have been increasingly examined for the trea...

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Autores principales:	Yoshiyuki Tago, Chiho Kobayashi, Mineko Ogura, Jutaro Wada, Sho Yamaguchi, Takashi Yamaguchi, Masahiro Hayashi, Tomoyuki Nakaishi, Hiroshi Kubo, Yasuyoshi Ueda
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/27be7c097a5e4194815dd4fc9c8dfa63
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spelling	oai:doaj.org-article:27be7c097a5e4194815dd4fc9c8dfa632021-12-02T13:57:59ZHuman amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation10.1038/s41598-021-81916-y2045-2322https://doaj.org/article/27be7c097a5e4194815dd4fc9c8dfa632021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-81916-yhttps://doaj.org/toc/2045-2322Abstract Acute graft-versus-host disease (GVHD) is characterized by severe tissue damage that is a life-threatening complication of allogeneic hematopoietic stem cell transplantation. Due to their immunosuppressive properties, mesenchymal stem cells (MSC) have been increasingly examined for the treatment of immune-related diseases. We aimed to assess the immunosuppressive effects of human amnion-derived MSC (AMSC) in a xenogeneic GVHD NOD/Shi-scid IL2rγnull mouse model using human peripheral blood mononuclear cells (PBMC). Additionally, we used human bone marrow-derived MSC (BMSC) as comparative controls to determine differences in immunomodulatory functions depending on the MSC origin. Administration of AMSC significantly prolonged survival, and reduced human tumor necrosis factor-α (TNF-α) concentration and percentage of programmed cell death protein-1 receptor (PD-1)+CD8+ T cell populations compared with in GVHD control mice. Furthermore, colonic inflammation score and percentage of human CD8+ T cell populations in AMSC-treated mice were significantly lower than in GVHD control and BMSC-treated mice. Interestingly, gene expression and protein secretion of the PD-1 ligands were higher in AMSC than in BMSC. These findings are the first to demonstrate that AMSC exhibit marked immunosuppression and delay acute GVHD progression by preventing T cell activation and proliferation via the PD-1 pathway.Yoshiyuki TagoChiho KobayashiMineko OguraJutaro WadaSho YamaguchiTakashi YamaguchiMasahiro HayashiTomoyuki NakaishiHiroshi KuboYasuyoshi UedaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yoshiyuki Tago Chiho Kobayashi Mineko Ogura Jutaro Wada Sho Yamaguchi Takashi Yamaguchi Masahiro Hayashi Tomoyuki Nakaishi Hiroshi Kubo Yasuyoshi Ueda Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation
description	Abstract Acute graft-versus-host disease (GVHD) is characterized by severe tissue damage that is a life-threatening complication of allogeneic hematopoietic stem cell transplantation. Due to their immunosuppressive properties, mesenchymal stem cells (MSC) have been increasingly examined for the treatment of immune-related diseases. We aimed to assess the immunosuppressive effects of human amnion-derived MSC (AMSC) in a xenogeneic GVHD NOD/Shi-scid IL2rγnull mouse model using human peripheral blood mononuclear cells (PBMC). Additionally, we used human bone marrow-derived MSC (BMSC) as comparative controls to determine differences in immunomodulatory functions depending on the MSC origin. Administration of AMSC significantly prolonged survival, and reduced human tumor necrosis factor-α (TNF-α) concentration and percentage of programmed cell death protein-1 receptor (PD-1)+CD8+ T cell populations compared with in GVHD control mice. Furthermore, colonic inflammation score and percentage of human CD8+ T cell populations in AMSC-treated mice were significantly lower than in GVHD control and BMSC-treated mice. Interestingly, gene expression and protein secretion of the PD-1 ligands were higher in AMSC than in BMSC. These findings are the first to demonstrate that AMSC exhibit marked immunosuppression and delay acute GVHD progression by preventing T cell activation and proliferation via the PD-1 pathway.
format	article
author	Yoshiyuki Tago Chiho Kobayashi Mineko Ogura Jutaro Wada Sho Yamaguchi Takashi Yamaguchi Masahiro Hayashi Tomoyuki Nakaishi Hiroshi Kubo Yasuyoshi Ueda
author_facet	Yoshiyuki Tago Chiho Kobayashi Mineko Ogura Jutaro Wada Sho Yamaguchi Takashi Yamaguchi Masahiro Hayashi Tomoyuki Nakaishi Hiroshi Kubo Yasuyoshi Ueda
author_sort	Yoshiyuki Tago
title	Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation
title_short	Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation
title_full	Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation
title_fullStr	Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation
title_full_unstemmed	Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation
title_sort	human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing t cell activation and proliferation
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/27be7c097a5e4194815dd4fc9c8dfa63
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Human amnion-derived mesenchymal stem cells attenuate xenogeneic graft-versus-host disease by preventing T cell activation and proliferation

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