دورية أكاديمية
The CD8 + T cell tolerance checkpoint triggers a distinct differentiation state defined by protein translation defects.
| العنوان: | The CD8 + T cell tolerance checkpoint triggers a distinct differentiation state defined by protein translation defects. |
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| المؤلفون: | Van Der Byl W; The Kirby Institute for Infection and Immunity, UNSW, Sydney, NSW, Australia; School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia., Nüssing S; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia., Peters TJ; Garvan Institute of Medical Research, Sydney, NSW, Australia; University of New South Wales Sydney, Sydney, NSW, Australia., Ahn A; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia., Li H; Department of Immunology, Weizmann Institute of Science, Rehovot, Israel., Ledergor G; Department of Immunology, Weizmann Institute of Science, Rehovot, Israel., David E; Department of Immunology, Weizmann Institute of Science, Rehovot, Israel., Koh AS; Department of Pathology, University of Chicago, Chicago, IL, USA., Wagle MV; Garvan Institute of Medical Research, Sydney, NSW, Australia; John Curtin School of Medical Research, ANU, Canberra, ACT, Australia., Deguit CDT; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia., de Menezes MN; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia., Travers A; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia., Sampurno S; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia., Ramsbottom KM; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia., Li R; Center for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA., Kallies A; The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia; Department of Microbiology and Immunology, The University of Melbourne, Melbourne, VIC, Australia., Beavis PA; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia., Jungmann R; Faculty of Physics and Center for Nanoscience, Ludwig Maximilian University, Munich, Germany; Max Planck Institute of Biochemistry, Martinsried, Germany., Bastings MMC; Institute of Materials, School of Engineering, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland; Interfaculty Bioengineering Institute, School of Engineering, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland., Belz GT; The Frazer Institute, The University of Queensland, Brisbane, QLD, Australia; Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia., Goel S; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia., Trapani JA; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia., Crabtree GR; Center for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA; Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA, USA., Chang HY; Center for Personal Dynamic Regulomes, Stanford University School of Medicine, Stanford, CA, USA., Amit I; Department of Immunology, Weizmann Institute of Science, Rehovot, Israel., Goodnow CC; School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia; Garvan Institute of Medical Research, Sydney, NSW, Australia., Luciani F; The Kirby Institute for Infection and Immunity, UNSW, Sydney, NSW, Australia; School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia. Electronic address: luciani@unsw.edu.au., Parish IA; Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia; John Curtin School of Medical Research, ANU, Canberra, ACT, Australia. Electronic address: ian.parish@petermac.org. |
| المصدر: | Immunity [Immunity] 2024 Jun 11; Vol. 57 (6), pp. 1324-1344.e8. Date of Electronic Publication: 2024 May 21. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Cell Press Country of Publication: United States NLM ID: 9432918 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4180 (Electronic) Linking ISSN: 10747613 NLM ISO Abbreviation: Immunity Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Cambridge, MA : Cell Press Original Publication: Cambridge, Mass. : Cell Press, c1994- |
| مواضيع طبية MeSH: | CD8-Positive T-Lymphocytes*/immunology , Cell Differentiation*/immunology , Receptors, Antigen, T-Cell*/metabolism , Receptors, Antigen, T-Cell*/immunology , Immune Tolerance*/immunology , Protein Biosynthesis*/immunology, Animals ; Mice ; Signal Transduction/immunology ; Mice, Inbred C57BL ; Autoantigens/immunology |
| مستخلص: | Peripheral CD8 + T cell tolerance is a checkpoint in both autoimmune disease and anti-cancer immunity. Despite its importance, the relationship between tolerance-induced states and other CD8 + T cell differentiation states remains unclear. Using flow cytometric phenotyping, single-cell RNA sequencing (scRNA-seq), and chromatin accessibility profiling, we demonstrated that in vivo peripheral tolerance to a self-antigen triggered a fundamentally distinct differentiation state separate from exhaustion, memory, and functional effector cells but analogous to cells defectively primed against tumors. Tolerant cells diverged early and progressively from effector cells, adopting a transcriptionally and epigenetically distinct state within 60 h of antigen encounter. Breaching tolerance required the synergistic actions of strong T cell receptor (TCR) signaling and inflammation, which cooperatively induced gene modules that enhanced protein translation. Weak TCR signaling during bystander infection failed to breach tolerance due to the uncoupling of effector gene expression from protein translation. Thus, tolerance engages a distinct differentiation trajectory enforced by protein translation defects. Competing Interests: Declaration of interests I.A.P. receives research funding from AstraZeneca and Bristol-Myers Squibb. H.Y.C. is a co-founder of Accent Therapeutics, Boundless Bio, Cartography Biosciences, and Orbital Therapeutics, and is an advisor for 10× Genomics, Arsenal Biosciences, Chroma Medicine, and Spring Discovery. (Copyright © 2024 Elsevier Inc. All rights reserved.) |
| فهرسة مساهمة: | Keywords: CD8(+) T cell; autoimmunity; cancer; differentiation; dysfunction; effector T cell; exhaustion; immunotherapy; stem-like T cell; tolerance |
| المشرفين على المادة: | 0 (Receptors, Antigen, T-Cell) 0 (Autoantigens) |
| تواريخ الأحداث: | Date Created: 20240522 Date Completed: 20240612 Latest Revision: 20240613 |
| رمز التحديث: | 20240614 |
| DOI: | 10.1016/j.immuni.2024.04.026 |
| PMID: | 38776918 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1097-4180 |
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| DOI: | 10.1016/j.immuni.2024.04.026 |