دورية أكاديمية

Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1.

التفاصيل البيبلوغرافية
العنوان: Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1.
المؤلفون: Patel CH; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Heikamp EB; Division of Hematology/Oncology, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; and., Xu W; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Sun IH; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Oh MH; Department of Immunobiology, Yale University, New Haven, CT., Sun IM; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Wen J; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Tam AJ; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Blosser RL; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD., Powell JD; Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney-Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD.
المصدر: Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2022 Dec 15; Vol. 209 (12), pp. 2287-2291.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print Cited Medium: Internet ISSN: 1550-6606 (Electronic) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE
أسماء مطبوعة: Publication: Bethesda, MD : American Association of Immunologists
Original Publication: Baltimore : Williams & Wilkins, c1950-
مواضيع طبية MeSH: CD8-Positive T-Lymphocytes* , Mechanistic Target of Rapamycin Complex 2*/metabolism , Memory T Cells* , Protein Serine-Threonine Kinases*/metabolism, Animals ; Mice ; Cell Differentiation ; Immunologic Memory/genetics ; Multiprotein Complexes/metabolism ; Sirolimus ; TOR Serine-Threonine Kinases/metabolism
مستخلص: The mechanistic target of rapamycin is an essential regulator of T cell metabolism and differentiation. In this study, we demonstrate that serum- and glucocorticoid-regulated kinase 1 (SGK1), a downstream node of mechanistic target of rapamycin complex 2 signaling, represses memory CD8+ T cell differentiation. During acute infections, murine SGK1-deficient CD8+ T cells adopt an early memory precursor phenotype leading to more long-lived memory T cells. Thus, SGK1-deficient CD8+ T cells demonstrate an enhanced recall capacity in response to reinfection and can readily reject tumors. Mechanistically, activation of SGK1-deficient CD8+ T cells results in decreased Foxo1 phosphorylation and increased nuclear translocation of Foxo1 to promote early memory development. Overall, SGK1 might prove to be a powerful target for enhancing the efficacy of vaccines and tumor immunotherapy.
(Copyright © 2022 by The American Association of Immunologists, Inc.)
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معلومات مُعتمدة: P41 EB028239 United States EB NIBIB NIH HHS; R01 AI077610 United States AI NIAID NIH HHS
المشرفين على المادة: EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2)
0 (Multiprotein Complexes)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
W36ZG6FT64 (Sirolimus)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
تواريخ الأحداث: Date Created: 20221205 Date Completed: 20230309 Latest Revision: 20240116
رمز التحديث: 20240117
مُعرف محوري في PubMed: PMC10065985
DOI: 10.4049/jimmunol.2100669
PMID: 36469844
قاعدة البيانات: MEDLINE
الوصف
تدمد:1550-6606
DOI:10.4049/jimmunol.2100669