دورية أكاديمية
Autophagy regulates T lymphocyte proliferation through selective degradation of the cell-cycle inhibitor CDKN1B/p27Kip1.
العنوان: | Autophagy regulates T lymphocyte proliferation through selective degradation of the cell-cycle inhibitor CDKN1B/p27Kip1. |
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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 |
تدمد: | 1554-8635 |
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DOI: | 10.1080/15548627.2015.1110666 |