Open AccessArp2/3 complex controls T cell homeostasis by maintaining surface TCR levels via regulating TCR+ endosome trafficking
Author(s) -
Ye Zhang,
Hao Shen,
Haifeng Liu,
Haiyun Feng,
Yan Liu,
Xiaoyan Zhu,
Xiaolong Liu
Publication year - 2017
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/s41598-017-08357-4
Subject(s) - immunological synapse , t cell receptor , microbiology and biotechnology , endosome , t cell , biology , homeostasis , immune system , immunology , intracellular
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.