دورية أكاديمية
أعرض في EDS

Metabolic reprogramming and dysregulated IL-17 production impairs CD4 T cell function post sepsis.

التفاصيل البيبلوغرافية
العنوان: Metabolic reprogramming and dysregulated IL-17 production impairs CD4 T cell function post sepsis.
المؤلفون: Assis PA; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA., Allen RM; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA., Schaller MA; Division of Pulmonary, Critical Care & Sleep Medicine, University of Florida College of Medicine, Gainesville, FL, USA., Kunkel SL; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA., Bermick JR; Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
المصدر: IScience [iScience] 2024 May 29; Vol. 27 (7), pp. 110114. Date of Electronic Publication: 2024 May 29 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101724038 Publication Model: eCollection Cited Medium: Internet ISSN: 2589-0042 (Electronic) Linking ISSN: 25890042 NLM ISO Abbreviation: iScience Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2018]-
مستخلص: Sepsis survivors are at high risk for infection-related rehospitalization and mortality for years following the resolution of the acute septic event. These infection-causing microorganisms generally do not cause disease in immunocompetent hosts, suggesting that the post-septic immune response is compromised. Given the importance of CD4 T cells in the development of long-lasting protective immunity, we analyzed their post-septic function. Here we showed that sepsis induced chronic increased and non-specific production of IL-17 by CD4 T cells, resulting in the inability to mount an effective immune response to a secondary pneumonia challenge. Altered cell function was associated with metabolic reprogramming, characterized by mitochondrial dysfunction and increased glycolysis. This metabolic reprogramming began during the acute septic event and persisted long after sepsis had resolved. Our findings reveal cell metabolism as a potential therapeutic target. Given the critical role of cell metabolism in the physiological and pathophysiological processes of immune cells, these findings reveal a potential new therapeutic target to help mitigate sepsis survivors' susceptibility to secondary infections.
Competing Interests: The authors declare no competing interests.
(© 2024 The Authors.)
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فهرسة مساهمة: Keywords: Components of the immune system; Immunology; Molecular biology; Physiology
تواريخ الأحداث: Date Created: 20240717 Latest Revision: 20240718
رمز التحديث: 20240718
مُعرف محوري في PubMed: PMC11251092
DOI: 10.1016/j.isci.2024.110114
PMID: 39015145
قاعدة البيانات: MEDLINE
الوصف
تدمد:2589-0042
DOI:10.1016/j.isci.2024.110114