Scientific Reports (Aug 2017)

Arp2/3 complex controls T cell homeostasis by maintaining surface TCR levels via regulating TCR+ endosome trafficking

  • Ye Zhang,
  • Hao Shen,
  • Haifeng Liu,
  • Haiyun Feng,
  • Yan Liu,
  • Xiaoyan Zhu,
  • Xiaolong Liu

DOI
https://doi.org/10.1038/s41598-017-08357-4
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 13

Abstract

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Abstract 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.