期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-08357-4
关键词
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资金
- National Basic Research Program of China [2013CB835300]
- National Natural Science Foundation of China [31530021, 31501193, 31621003]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB19000000]
- Youth Innovation Promotion Association of Chinese Academy of Sciences
T cell receptor (TCR) signaling is important for T cell homeostasis and function. However, how surface TCR levels are regulated and its biological significance on T cells remains largely unknown. Here, we show that the T cell-specific deletion of Arpc2, a component of Arp2/3 complex, results in compromised peripheral T cell homeostasis. Arp2/3 complex-nucleated actin filaments are essential for maintaining surface TCR levels by regulating TCR+ endosome trafficking in resting state and controlling polarization of TCR+ endosomes during immune synapse formation in T cells. Additionally, Arpc2-TKO T cells are unable to form immune synapse. Interestingly, defected T cell homeostasis is caused by reduced surface TCR levels but not impaired immune synapse formation. Collectively, our findings suggest that Arp2/3 complex-nucleated actin filaments are required for maintaining surface TCR levels via regulating TCR+ endosome trafficking which is essential for T cell homeostasis.
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