التفاصيل البيبلوغرافية
العنوان: |
NIX-Mediated Mitophagy Promotes Effector Memory Formation in Antigen-Specific CD8+ T Cells |
المؤلفون: |
Shubhranshu S. Gupta, Robert Sharp, Colby Hofferek, Le Kuai, Gerald W. Dorn, II, Jin Wang, Min Chen |
المصدر: |
Cell Reports, Vol 29, Iss 7, Pp 1862-1877.e7 (2019) |
بيانات النشر: |
Elsevier, 2019. |
سنة النشر: |
2019 |
المجموعة: |
LCC:Biology (General) |
مصطلحات موضوعية: |
Biology (General), QH301-705.5 |
الوصف: |
Summary: Autophagy plays a critical role in the maintenance of immunological memory. However, the molecular mechanisms involved in autophagy-regulated effector memory formation in CD8+ T cells remain unclear. Here we show that deficiency in NIX-dependent mitophagy leads to metabolic defects in effector memory T cells. Deletion of NIX caused HIF1α accumulation and altered cellular metabolism from long-chain fatty acid to short/branched-chain fatty acid oxidation, thereby compromising ATP synthesis during effector memory formation. Preventing HIF1α accumulation restored long-chain fatty acid metabolism and effector memory formation in antigen-specific CD8+ T cells. Our study suggests that NIX-mediated mitophagy is critical for effector memory formation in T cells. : Gupta et al. demonstrate that mitophagy mediated by NIX, a mitochondrial outer membrane protein, plays a critical role in CD8+ T cell effector memory formation by regulating mitochondrial superoxide-dependent HIF1α protein accumulation and fatty acid metabolism. These findings elucidate the molecular mechanisms regulating T cell effector memory formation against viruses. Keywords: NIX, mitophagy, autophagy, CD8+ T cells, effector memory cells, HIF1α, fatty acid metabolism, long-chain fatty acid oxidation, short/branched-chain fatty acid oxidation, mitochondrial superoxide |
نوع الوثيقة: |
article |
وصف الملف: |
electronic resource |
اللغة: |
English |
تدمد: |
2211-1247 |
Relation: |
http://www.sciencedirect.com/science/article/pii/S2211124719313324; https://doaj.org/toc/2211-1247 |
DOI: |
10.1016/j.celrep.2019.10.032 |
URL الوصول: |
https://doaj.org/article/05db3314bc774a509a992253e0f81ea7 |
رقم الانضمام: |
edsdoj.05db3314bc774a509a992253e0f81ea7 |
قاعدة البيانات: |
Directory of Open Access Journals |