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DOI10.1073/pnas.2023752118
Fever supports CD8+ effector T cell responses by promoting mitochondrial translation
OSullivan D.; Stanczak M.A.; Villa M.; Uhl F.M.; Corrado M.; Klein Geltink R.I.; Sanin D.E.; Apostolova P.; Rana N.; Edwards-Hicks J.; Grzes K.M.; Kabat A.M.; Kyle R.L.; Fabri M.; Curtis J.D.; Buck M.D.; Patterson A.E.; Regina A.; Field C.S.; Baixauli F.; Puleston D.J.; Pearce E.J.; Zeiser R.; Pearce E.L.
发表日期2021
ISSN0027-8424
卷号118期号:25
英文摘要Fever can provide a survival advantage during infection. Metabolic processes are sensitive to environmental conditions, but the effect of fever on T cell metabolism is not well characterized. We show that in activated CD8+ T cells, exposure to febrile temperature (39 °C) augmented metabolic activity and T cell effector functions, despite having a limited effect on proliferation or activation marker expression. Transcriptional profiling revealed an up-regulation of mitochondrial pathways, which was consistent with increased mass and metabolism observed in T cells exposed to 39 °C. Through in vitro and in vivo models, we determined that mitochondrial translation is integral to the enhanced metabolic activity and function of CD8+ T cells exposed to febrile temperature. Transiently exposing donor lymphocytes to 39 °C prior to infusion in a myeloid leukemia mouse model conferred enhanced therapeutic efficacy, raising the possibility that exposure of T cells to febrile temperatures could have clinical potential. © 2021 National Academy of Sciences. All rights reserved.
英文关键词fever; immunology; metabolism; mitochondria; T cell
语种英语
scopus关键词CD28 antigen; CD3 antigen; CD8 antigen; cytochrome c oxidase; gamma interferon; interleukin 1beta; prostaglandin E2; tumor necrosis factor; animal cell; animal experiment; animal model; antileukemic activity; Article; body temperature; bone marrow transplantation; CD8+ T lymphocyte; cell metabolism; cell proliferation; controlled study; cytokine production; donor lymphocyte infusion; effector cell; fever; genetic transcription; in vitro study; in vivo study; lymphocyte function; mitochondrion; mouse; myeloid leukemia; nonhuman; nuclear reprogramming; oxidative phosphorylation; upregulation
来源期刊Proceedings of the National Academy of Sciences of the United States of America
文献类型期刊论文
条目标识符http://gcip.llas.ac.cn/handle/2XKMVOVA/238513
作者单位Max Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, 79108, Germany; Department of Hematology,, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Freiburg im Breisgau, 79106, Germany; Faculty of Biology, University of Freiburg, Freiburg im Breisgau, 79104, Germany; Department of Dermatology and Venereology, University of Cologne, Cologne, 50937, Germany; Department of Life Sciences, University of Trieste, Trieste, 34128, Italy
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GB/T 7714
OSullivan D.,Stanczak M.A.,Villa M.,et al. Fever supports CD8+ effector T cell responses by promoting mitochondrial translation[J],2021,118(25).
APA OSullivan D..,Stanczak M.A..,Villa M..,Uhl F.M..,Corrado M..,...&Pearce E.L..(2021).Fever supports CD8+ effector T cell responses by promoting mitochondrial translation.Proceedings of the National Academy of Sciences of the United States of America,118(25).
MLA OSullivan D.,et al."Fever supports CD8+ effector T cell responses by promoting mitochondrial translation".Proceedings of the National Academy of Sciences of the United States of America 118.25(2021).
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