Characterization, biology, and expansion of regulatory T cells in the Cynomolgus macaque for preclinical studies.

animal models: nonhuman primate basic (laboratory) research/science cellular transplantation (nonislet) graft survival immune regulation immunobiology immunosuppression/immune modulation tolerance: chimerism translational research/science

Journal

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
ISSN: 1600-6143
Titre abrégé: Am J Transplant
Pays: United States
ID NLM: 100968638

Informations de publication

Date de publication:
08 2019
Historique:
received: 05 09 2018
revised: 16 01 2019
accepted: 04 02 2019
pubmed: 16 2 2019
medline: 1 9 2020
entrez: 16 2 2019
Statut: ppublish

Résumé

Reliable in vitro expansion protocols of regulatory T cells (Tregs) are needed for clinical use. We studied the biology of Mauritian Cynomolgus macaque (MCM) Tregs and developed four in vitro Treg expansion protocols for translational studies. Tregs expanded 3000-fold when artificial antigen presenting cells (aAPCs) expressing human CD80, CD58 and CD32 were used throughout the culture. When donor peripheral blood mononuclear cells (PBMCs) were used as the single source of APCs followed by aAPCs, Tregs expanded 2000-fold. Tregs from all protocols suppressed the proliferation of anti-CD2CD3CD28 bead-stimulated autologous PBMCs albeit with different potencies, varying from 1:2-1:4 Treg:PBMC ratios, up to >1:32. Reculture of cryopreserved Tregs permitted reexpansion with improved suppressive activity. Occasionally, CD8 contamination was observed and resolved by resorting. Specificity studies showed greater suppression of stimulation by anti-CD2CD3CD28 beads of PBMCs from the same donor used for stimulation during the Treg cultures and of autologous cells than of third-party PBMC responders. Similar to humans, the Treg-specific demethylated region (TSDR) within the Foxp3 locus correlated with suppressive activity and expression of Foxp3. Contrary to humans, FoxP3 expression did not correlate with CD45RA or CD127 expression. In summary, we have characterized MCM Tregs and developed four Treg expansion protocols that can be used for preclinical applications.

Identifiants

pubmed: 30768842
doi: 10.1111/ajt.15313
pmc: PMC6658340
mid: NIHMS1011949
pii: S1600-6135(22)09185-7
doi:

Substances chimiques

FOXP3 protein, human 0
Forkhead Transcription Factors 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2186-2198

Subventions

Organisme : Columbia University Departments of Medicine and Surgery
Pays : International
Organisme : Columbia University Core award
Pays : International
Organisme : Irving Pilot Translational Science award for new investigators
Pays : International
Organisme : NIH HHS
ID : R01 OD017949
Pays : United States
Organisme : NIH HHS
ID : S10 OD020056
Pays : United States
Organisme : Banting Foundation
Pays : International

Informations de copyright

© 2019 The American Society of Transplantation and the American Society of Transplant Surgeons.

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Auteurs

Paula Alonso-Guallart (P)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.

Jonah S Zitsman (JS)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.

Jeffrey Stern (J)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.

Sigal B Kofman (SB)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.

David Woodland (D)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.

Siu-Hong Ho (SH)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.

Hugo P Sondermeijer (HP)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.
Department of Physiology, Maastricht University, Maastricht, The Netherlands.

Leo Bühler (L)

Department of Surgery, University Hospital of Geneva, Switzerland.

Adam Griesemer (A)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.
Department of Surgery, Columbia University Medical Center, New York, New York.

Megan Sykes (M)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.
Department of Surgery, Columbia University Medical Center, New York, New York.
Department of Microbiology and Immunology, Columbia University Medical Center, New York, New York.

Raimon Duran-Struuck (R)

Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.
Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania.

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