Analysis of therapeutic potential of monocytic myeloid-derived suppressor cells in cardiac allotransplantation.


Journal

Transplant immunology
ISSN: 1878-5492
Titre abrégé: Transpl Immunol
Pays: Netherlands
ID NLM: 9309923

Informations de publication

Date de publication:
08 2021
Historique:
received: 03 12 2020
revised: 12 04 2021
accepted: 06 05 2021
pubmed: 12 5 2021
medline: 28 12 2021
entrez: 11 5 2021
Statut: ppublish

Résumé

Myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) are attractive immune cells to induce immune tolerance. To explore a strategy for improving the efficacy of MDSC therapies, we examined the impact of adoptive transfer of several types of MDSCs on graft rejection in a murine heart transplantation model. We analyzed the effects of induced syngeneic and allogeneic bone marrow-derived MDSCs (BM-MDSCs) on graft survival and suppressive capacity. We also compared the ability of syngeneic monocytic MDSCs (Mo-MDSCs) and polymorphonuclear MDSCs (PMN-MDSCs) to inhibit graft rejection and investigated the suppression mechanisms. Both syngeneic and allogeneic donor- or allogeneic third-party-derived BM-MDSCs prolonged graft survival, although syngeneic BM-MDSCs inhibited anti-donor immune responses most effectively in vitro. Syngeneic Mo-MDSCs, rather than PMN-MDSCs, were responsible for immune suppression through downregulating inducible nitric oxide synthase (iNOS) and expanded naturally occurring thymic originated Treg (nTreg) in vitro. Adoptive transfer of Mo-MDSCs, but not PMN-MDSCs, prolonged graft survival and increased Treg infiltration into the graft heart. Recipient-derived Mo-MDSCs are most effective in prolonging graft survival via inhibiting T cell response and nTreg infiltration.

Sections du résumé

BACKGROUND
Myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) are attractive immune cells to induce immune tolerance. To explore a strategy for improving the efficacy of MDSC therapies, we examined the impact of adoptive transfer of several types of MDSCs on graft rejection in a murine heart transplantation model.
METHODS
We analyzed the effects of induced syngeneic and allogeneic bone marrow-derived MDSCs (BM-MDSCs) on graft survival and suppressive capacity. We also compared the ability of syngeneic monocytic MDSCs (Mo-MDSCs) and polymorphonuclear MDSCs (PMN-MDSCs) to inhibit graft rejection and investigated the suppression mechanisms.
RESULTS
Both syngeneic and allogeneic donor- or allogeneic third-party-derived BM-MDSCs prolonged graft survival, although syngeneic BM-MDSCs inhibited anti-donor immune responses most effectively in vitro. Syngeneic Mo-MDSCs, rather than PMN-MDSCs, were responsible for immune suppression through downregulating inducible nitric oxide synthase (iNOS) and expanded naturally occurring thymic originated Treg (nTreg) in vitro. Adoptive transfer of Mo-MDSCs, but not PMN-MDSCs, prolonged graft survival and increased Treg infiltration into the graft heart.
CONCLUSION
Recipient-derived Mo-MDSCs are most effective in prolonging graft survival via inhibiting T cell response and nTreg infiltration.

Identifiants

pubmed: 33975012
pii: S0966-3274(21)00045-9
doi: 10.1016/j.trim.2021.101405
pii:
doi:

Substances chimiques

Nitric Oxide Synthase Type II EC 1.14.13.39

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

101405

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.

Auteurs

Keiichi Fujimoto (K)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan; Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan. Electronic address: k-fujimoto@juntendo.ac.jp.

Koichiro Uchida (K)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan; Advanced Research Institute for Health Science, Juntendo University, Tokyo, Japan. Electronic address: k-uchida@juntendo.ac.jp.

Enzhi Yin (E)

Department of Surgery, Teikyo University, Tokyo, Japan.

Jun Zhu (J)

Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan. Electronic address: j.zhu.gx@juntendo.ac.jp.

Yuko Kojima (Y)

Laboratory of Morphology and Image Analysis, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: kojima-y@juntendo.ac.jp.

Masateru Uchiyama (M)

Department of Surgery, Teikyo University, Tokyo, Japan.

Yasuto Yamamoto (Y)

Department of Surgery, Teikyo University, Tokyo, Japan.

Hisashi Bashuda (H)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: bashuda@juntendo.ac.jp.

Ryu Matsumoto (R)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: r.matsumoto.ew@juntendo.ac.jp.

Koji Tokushige (K)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: k.tokushige.dj@juntendo.ac.jp.

Masaki Harada (M)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: m.harada.tk@juntendo.ac.jp.

Takenori Inomata (T)

Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan. Electronic address: tinoma@juntendo.ac.jp.

Jiro Kitaura (J)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: j-kitaura@juntendo.ac.jp.

Akira Murakami (A)

Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan. Electronic address: amurak@juntendo.ac.jp.

Ko Okumura (K)

Atopy Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan; Department of Biofunctional Microbiota, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: kokumura@juntendo.ac.jp.

Kazuyoshi Takeda (K)

Department of Biofunctional Microbiota, Juntendo University Graduate School of Medicine, Tokyo, Japan; Division of Cell Biology, Biomedical Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan. Electronic address: ktakeda@juntendo.ac.jp.

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