دورية أكاديمية
أعرض في EDS

Autophagy regulates T lymphocyte proliferation through selective degradation of the cell-cycle inhibitor CDKN1B/p27Kip1.

التفاصيل البيبلوغرافية
العنوان: Autophagy regulates T lymphocyte proliferation through selective degradation of the cell-cycle inhibitor CDKN1B/p27Kip1.
المؤلفون: Jia W; a Department of Immunology ; Duke University Medical Center ; Durham ; NC , USA., He MX; a Department of Immunology ; Duke University Medical Center ; Durham ; NC , USA., McLeod IX; a Department of Immunology ; Duke University Medical Center ; Durham ; NC , USA., Guo J; a Department of Immunology ; Duke University Medical Center ; Durham ; NC , USA., Ji D; a Department of Immunology ; Duke University Medical Center ; Durham ; NC , USA., He YW; a Department of Immunology ; Duke University Medical Center ; Durham ; NC , USA.
المصدر: Autophagy [Autophagy] 2015; Vol. 11 (12), pp. 2335-45.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Taylor & Francis Country of Publication: United States NLM ID: 101265188 Publication Model: Print Cited Medium: Internet ISSN: 1554-8635 (Electronic) Linking ISSN: 15548627 NLM ISO Abbreviation: Autophagy Subsets: MEDLINE
أسماء مطبوعة: Publication: 2015- : Philadelphia, PA : Taylor & Francis
Original Publication: Georgetown, TX : Landes Bioscience, 2005-
مواضيع طبية MeSH: Autophagy/*physiology , Cell Cycle Checkpoints/*physiology , Cell Proliferation/*physiology , Cyclin-Dependent Kinase Inhibitor p27/*metabolism , Lymphocyte Activation/*immunology , T-Lymphocytes/*cytology, Animals ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Homeostasis/physiology ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins/metabolism ; Mitochondria/metabolism ; T-Lymphocytes/immunology
مستخلص: The highly conserved cellular degradation pathway, macroautophagy, regulates the homeostasis of organelles and promotes the survival of T lymphocytes. Previous results indicate that Atg3-, Atg5-, or Pik3c3/Vps34-deficient T cells cannot proliferate efficiently. Here we demonstrate that the proliferation of Atg7-deficient T cells is defective. By using an adoptive transfer and Listeria monocytogenes (LM) mouse infection model, we found that the primary immune response against LM is intrinsically impaired in autophagy-deficient CD8(+) T cells because the cell population cannot expand after infection. Autophagy-deficient T cells fail to enter into S-phase after TCR stimulation. The major negative regulator of the cell cycle in T lymphocytes, CDKN1B, is accumulated in autophagy-deficient naïve T cells and CDKN1B cannot be degraded after TCR stimulation. Furthermore, our results indicate that genetic deletion of one allele of CDKN1B in autophagy-deficient T cells restores proliferative capability and the cells can enter into S-phase after TCR stimulation. Finally, we found that natural CDKN1B forms polymers and is physiologically associated with the autophagy receptor protein SQSTM1/p62 (sequestosome 1). Collectively, autophagy is required for maintaining the expression level of CDKN1B in naïve T cells and selectively degrades CDKN1B after TCR stimulation.
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معلومات مُعتمدة: AI074754 United States AI NIAID NIH HHS; AI074944 United States AI NIAID NIH HHS
فهرسة مساهمة: Keywords: ATG3; ATG7; CDKN1B; T lymphocytes; autophagy; proliferation
المشرفين على المادة: 0 (Cdkn1b protein, mouse)
0 (Microtubule-Associated Proteins)
147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
تواريخ الأحداث: Date Created: 20151117 Date Completed: 20161031 Latest Revision: 20181113
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4835188
DOI: 10.1080/15548627.2015.1110666
PMID: 26569626
قاعدة البيانات: MEDLINE
الوصف
تدمد:1554-8635
DOI:10.1080/15548627.2015.1110666