期刊
CELL REPORTS
卷 25, 期 11, 页码 3059-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.11.018
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资金
- Italian Ministry of Health [GR-2016-02363749, GR-2011-02351643]
- AIRC [IG-2017 19784, IG-2014 15199, IG-2017 19939, IG-2017 19826]
- European Research Council grant menTORingTregs [310496]
- Fondazione Italiana Sclerosi Multipla (FISM) [2016/R/18]
- Telethon [GGP17086]
- MIUR [RF-2010-2310438, RF 2010-2318269]
- MIUR PRIN [2010LC747T_004]
- FISM onlus [2015/R/04]
- Istituto Pasteur Italia -Fondazione Cenci Bolognetti
- Fondazione Roma [NCDS-2013-000000345]
- International Network Institut Pasteur [PTR 20-16]
- AIRC MultiUnit-5 per Mille [12162]
- FIRB-2011/13 [RBAP10TPXK]
Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and accumulation at tumor sites. Moreover, the observed Drp1-dependent imbalance toward a memory-like phenotype favors T cell exhaustion in the tumor microenvironment. All of these findings support a crucial role for Drp1 in several processes during T cell development and in anti-tumor immune-surveillance.
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