دورية أكاديمية
أعرض في EDS

ER-associated degradation adapter Sel1L is required for CD8 + T cell function and memory formation following acute viral infection.

التفاصيل البيبلوغرافية
العنوان: ER-associated degradation adapter Sel1L is required for CD8 + T cell function and memory formation following acute viral infection.
المؤلفون: Correa-Medero LO; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Jankowski SE; University of Michigan, Ann Arbor, MI 48109, USA., Hong HS; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Armas ND; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Vijendra AI; University of Michigan, Ann Arbor, MI 48109, USA., Reynolds MB; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Fogo GM; Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA., Awad D; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA., Dils AT; Division of Hematology and Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA., Inoki KA; University of Michigan, Ann Arbor, MI 48109, USA., Williams RG; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Ye AM; University of Michigan, Ann Arbor, MI 48109, USA., Svezhova N; Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Gomez-Rivera F; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Collins KL; Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA; Cellular and Molecular Biology Graduate Program, University of Michigan, Ann Arbor, MI 48109, USA., O'Riordan MX; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA., Sanderson TH; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA., Lyssiotis CA; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA., Carty SA; Division of Hematology and Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA; Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: scarty@umich.edu.
المصدر: Cell reports [Cell Rep] 2024 May 28; Vol. 43 (5), pp. 114156. Date of Electronic Publication: 2024 Apr 29.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101573691 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2211-1247 (Electronic) NLM ISO Abbreviation: Cell Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, c 2012-
مواضيع طبية MeSH: CD8-Positive T-Lymphocytes*/immunology , CD8-Positive T-Lymphocytes*/metabolism , Endoplasmic Reticulum Stress* , Endoplasmic Reticulum-Associated Degradation* , Immunologic Memory*, Animals ; Humans ; Mice ; Acute Disease ; Intracellular Signaling Peptides and Proteins ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic Choriomeningitis/virology ; Lymphocytic Choriomeningitis/pathology ; Mice, Inbred C57BL ; Proteins ; RNA-Binding Proteins/metabolism ; RNA-Binding Proteins/genetics ; Male ; Female
مستخلص: The maintenance of antigen-specific CD8 + T cells underlies the efficacy of vaccines and immunotherapies. Pathways contributing to CD8 + T cell loss are not completely understood. Uncovering the pathways underlying the limited persistence of CD8 + T cells would be of significant benefit for developing novel strategies of promoting T cell persistence. Here, we demonstrate that murine CD8 + T cells experience endoplasmic reticulum (ER) stress following activation and that the ER-associated degradation (ERAD) adapter Sel1L is induced in activated CD8 + T cells. Sel1L loss limits CD8 + T cell function and memory formation following acute viral infection. Mechanistically, Sel1L is required for optimal bioenergetics and c-Myc expression. Finally, we demonstrate that human CD8 + T cells experience ER stress upon activation and that ER stress is negatively associated with improved T cell functionality in T cell-redirecting therapies. Together, these results demonstrate that ER stress and ERAD are important regulators of T cell function and persistence.
Competing Interests: Declaration of interests In the past three years, C.A.L. has consulted for Astellas Pharmaceuticals, Odyssey Therapeutics, Third Rock Ventures, and T-Knife Therapeutics and is an inventor on patents pertaining to Kras-regulated metabolic pathways, redox control pathways in pancreatic cancer, and therapeutically targeting the GOT1-ME1 pathway (US Patent no. 2015126580-A1, 05/07/2015; US Patent no. 20190136238, 05/09/2019; International Patent no. WO2013177426-A2, 04/23/2015).
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: F99 AG079793 United States AG NIA NIH HHS; 75N92020D00005 United States HL NHLBI NIH HHS; 75N93022D00005 United States AI NIAID NIH HHS; R01 AI165533 United States AI NIAID NIH HHS; 75N95020D00005 United States DA NIDA NIH HHS; T32 AI007413 United States AI NIAID NIH HHS; T32 CA140044 United States CA NCI NIH HHS; R01 AI157384 United States AI NIAID NIH HHS; 75N93023D00005 United States AI NIAID NIH HHS; P30 CA046592 United States CA NCI NIH HHS; F31 NS124280 United States NS NINDS NIH HHS; 75N99020D00005 United States OF ORFDO NIH HHS; R01 NS120322 United States NS NINDS NIH HHS
فهرسة مساهمة: Keywords: CD8 T cell; CP: Immunology; ER stress; ERAD; Myc; T cell memory; immunometabolism; protein homeostasis
المشرفين على المادة: 0 (Intracellular Signaling Peptides and Proteins)
0 (Proteins)
0 (RNA-Binding Proteins)
0 (Sel1h protein, mouse)
0 (SEL1L protein, human)
تواريخ الأحداث: Date Created: 20240430 Date Completed: 20240531 Latest Revision: 20240901
رمز التحديث: 20240901
مُعرف محوري في PubMed: PMC11194752
DOI: 10.1016/j.celrep.2024.114156
PMID: 38687642
قاعدة البيانات: MEDLINE
الوصف
تدمد:2211-1247
DOI:10.1016/j.celrep.2024.114156