Please use this identifier to cite or link to this item:
https://ahro.austin.org.au/austinjspui/handle/1/30746
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DC Field | Value | Language |
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dc.contributor.author | Tsui, Carlson | - |
dc.contributor.author | Kretschmer, Lorenz | - |
dc.contributor.author | Rapelius, Svenja | - |
dc.contributor.author | Gabriel, Sarah S | - |
dc.contributor.author | Chisanga, David | - |
dc.contributor.author | Knöpper, Konrad | - |
dc.contributor.author | Utzschneider, Daniel T | - |
dc.contributor.author | Nüssing, Simone | - |
dc.contributor.author | Liao, Yang | - |
dc.contributor.author | Mason, Teisha | - |
dc.contributor.author | Torres, Santiago Valle | - |
dc.contributor.author | Wilcox, Stephen A | - |
dc.contributor.author | Kanev, Krystian | - |
dc.contributor.author | Jarosch, Sebastian | - |
dc.contributor.author | Leube, Justin | - |
dc.contributor.author | Nutt, Stephen L | - |
dc.contributor.author | Zehn, Dietmar | - |
dc.contributor.author | Parish, Ian A | - |
dc.contributor.author | Kastenmüller, Wolfgang | - |
dc.contributor.author | Shi, Wei | - |
dc.contributor.author | Buchholz, Veit R | - |
dc.contributor.author | Kallies, Axel | - |
dc.date | 2022 | - |
dc.date.accessioned | 2022-08-25T05:17:39Z | - |
dc.date.available | 2022-08-25T05:17:39Z | - |
dc.date.issued | 2022-08-17 | - |
dc.identifier.citation | Nature 2022; 609(7926): 354-360 | en |
dc.identifier.uri | https://ahro.austin.org.au/austinjspui/handle/1/30746 | - |
dc.description.abstract | CD8+ T cells that respond to chronic viral infections or cancer are characterized by the expression of inhibitory receptors such as programmed cell death protein 1 (PD-1) and by the impaired production of cytokines. This state of restrained functionality-which is referred to as T cell exhaustion1,2-is maintained by precursors of exhausted T (TPEX) cells that express the transcription factor T cell factor 1 (TCF1), self-renew and give rise to TCF1- exhausted effector T cells3-6. Here we show that the long-term proliferative potential, multipotency and repopulation capacity of exhausted T cells during chronic infection are selectively preserved in a small population of transcriptionally distinct CD62L+ TPEX cells. The transcription factor MYB is not only essential for the development of CD62L+ TPEX cells and maintenance of the antiviral CD8+ T cell response, but also induces functional exhaustion and thereby prevents lethal immunopathology. Furthermore, the proliferative burst in response to PD-1 checkpoint inhibition originates exclusively from CD62L+ TPEX cells and depends on MYB. Our findings identify CD62L+ TPEX cells as a stem-like population that is central to the maintenance of long-term antiviral immunity and responsiveness to immunotherapy. Moreover, they show that MYB is a transcriptional orchestrator of two fundamental aspects of exhausted T cell responses: the downregulation of effector function and the long-term preservation of self-renewal capacity. | en |
dc.language.iso | eng | - |
dc.title | MYB orchestrates T cell exhaustion and response to checkpoint inhibition. | en |
dc.type | Journal Article | en |
dc.identifier.journaltitle | Nature | en |
dc.identifier.affiliation | The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | Department of Medical Biology, University of Melbourne, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | School of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | Department of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | School of Computing and Information Systems, University of Melbourne, Melbourne, Victoria, Australia.. | en |
dc.identifier.affiliation | Olivia Newton-John Cancer Research Institute | en |
dc.identifier.affiliation | Institute for Medical Microbiology, Immunology and Hygiene, School of Medicine, Technical University of Munich (TUM), Munich, Germany.. | en |
dc.identifier.affiliation | Würzburg Institute of Systems Immunology, Max Planck Research Group, Julius-Maximilians-Universität Würzburg, Würzburg, Germany.. | en |
dc.identifier.affiliation | Division of Animal Physiology and Immunology, School of Life Sciences Weihenstephan, Technical University of Munich (TUM), Freising, Germany.. | en |
dc.identifier.pubmeduri | https://pubmed.ncbi.nlm.nih.gov/35978192/ | en |
dc.identifier.doi | 10.1038/s41586-022-05105-1 | en |
dc.type.content | Text | en |
dc.identifier.orcid | http://orcid.org/0000-0003-0642-814X | en |
dc.identifier.orcid | http://orcid.org/0000-0003-0987-8429 | en |
dc.identifier.orcid | http://orcid.org/0000-0002-0421-3957 | en |
dc.identifier.orcid | http://orcid.org/0000-0003-2076-2160 | en |
dc.identifier.orcid | http://orcid.org/0000-0003-2205-9057 | en |
dc.identifier.orcid | http://orcid.org/0000-0002-9746-2839 | en |
dc.identifier.orcid | http://orcid.org/0000-0002-2908-8590 | en |
dc.identifier.orcid | http://orcid.org/0000-0002-0020-6637 | en |
dc.identifier.orcid | http://orcid.org/0000-0003-1393-8527 | en |
dc.identifier.orcid | http://orcid.org/0000-0003-3528-478X | en |
dc.identifier.orcid | http://orcid.org/0000-0002-3835-1485 | en |
dc.identifier.orcid | http://orcid.org/0000-0003-0441-3913 | en |
dc.identifier.orcid | http://orcid.org/0000-0002-6312-6968 | en |
dc.identifier.orcid | http://orcid.org/0000-0003-1182-7735 | en |
dc.identifier.pubmedid | 35978192 | - |
item.languageiso639-1 | en | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
item.openairetype | Journal Article | - |
Appears in Collections: | Journal articles |
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