| Literature DB >> 28470889 |
K L Hippen1, R S O'Connor2, A M Lemire1, A Saha1, E A Hanse3, N C Tennis1, S C Merkel1, A Kelekar3, J L Riley4, B L Levine4, C H June4, L A Turka5, L S Kean6,7, M L MacMillan1, J S Miller8, J E Wagner1, D H Munn9, B R Blazar1.
Abstract
Thymic regulatory T cells (tTregs) and induced regulatory T cells (iTregs) suppress murine acute graft-versus-host disease (GVHD). Previously, we demonstrated that the plasmacytoid dendritic cell indoleamine 2,3-dioxygenase (IDO) fosters the in vitro development of human iTregs via tryptophan depletion and kynurenine (Kyn) metabolites. We now show that stimulation of naïve CD4+ T cells in low tryptophan (low Trp) plus Kyn supports human iTreg generation. In vitro, low Trp + Kyn iTregs and tTregs potently suppress T effector cell proliferation equivalently but are phenotypically distinct. Compared with tTregs or T effector cells, bioenergetics profiling reveals that low Trp + Kyn iTregs have increased basal glycolysis and oxidative phosphorylation and use glutaminolysis as an energy source. Low Trp + Kyn iTreg viability was reliant on interleukin (IL)-2 in vitro. Although in vivo IL-2 administration increased low Trp + Kyn iTreg persistence on adoptive transfer into immunodeficient mice given peripheral blood mononuclear cells to induce GVHD, IL-2-supported iTregs did not improve recipient survival. We conclude that low Trp + Kyn create suppressive iTregs that have high metabolic needs that will need to be addressed before clinical translation.Entities:
Keywords: T cell biology; basic (laboratory) research/science; bone marrow/hematopoietic stem cell transplantation; graft-versus-host disease (GVHD); immune regulation; immunosuppression/immune modulation; tolerance: clinical; translational research/science; xenotransplantation
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Year: 2017 PMID: 28470889 PMCID: PMC5671378 DOI: 10.1111/ajt.14338
Source DB: PubMed Journal: Am J Transplant ISSN: 1600-6135 Impact factor: 8.086