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Peer-reviewedCC BY-NC-ND 4.0NPJ Systems Biology and Applications

Sleep restriction reprograms systemic immunity through NK and T cell crosstalk

  • Zhengyang Qiu1,2
  • Jichen Jin1,3
  • Pengqi Zhang1,3
  • Chen Li4
  • Yongmei Xi1,3
4 affiliations
  1. 1Institute of Genetics, Zhejiang University International School of Medicine, Hangzhou, Zhejiang China
  2. 2School of Computer Science and Technology, Beijing Jiaotong University, Beijing, China
  3. 3Center for Genetic Medicine, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, Zhejiang China
  4. 4Department of Human Genetics, and Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, China
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Abstract

Insufficient sleep is a recognized risk factor for inflammatory diseases, yet how sleep loss functionally perturbs immune regulation remains unclear. Here, we apply a multi-omics framework combining two-sample Mendelian randomization, sleep-restriction intervention microarray, and PBMC single-cell profiling to dissect immune consequences of sleep loss. Mendelian randomization associated genetically proxied sleeplessness/insomnia symptoms with alterations in 162 plasma proteins and increased risk across 94 clinical diagnosis traits. Gene expression microarray after sleep restriction confirmed immune activation and stress-response programs. Single-cell RNA sequencing revealed PBMC remodeling with increased NK/NKT cells and decreased γδ T cells and dendritic cells, alongside pro-inflammatory pathway activity. Ligand–receptor analysis identified altered intercellular communication patterns, characterized by increasing signals to NK cells and enhancing NK–T cell-associated interfaces. These findings nominate dysregulated NK cell–T cell crosstalk as a putative mechanism underlying sleep-related inflammation and provide prioritized targets for future validation.

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Cite

BibTeXRIS
BibTeX
@article{qiu2026sleep,
  title = {{Sleep restriction reprograms systemic immunity through NK and T cell crosstalk}},
  author = {Zhengyang Qiu and Jichen Jin and Pengqi Zhang and Chen Li and Yongmei Xi},
  journal = {NPJ Systems Biology and Applications},
  year = {2026},
  month = jul,
  doi = {10.1038/s41540-026-00787-z},
  url = {https://doi.org/10.1038/s41540-026-00787-z},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Sleep restriction reprograms systemic immunity through NK and T cell crosstalk
AU  - Zhengyang Qiu
AU  - Jichen Jin
AU  - Pengqi Zhang
AU  - Chen Li
AU  - Yongmei Xi
PY  - 2026
DA  - 2026/07/14
JO  - NPJ Systems Biology and Applications
DO  - 10.1038/s41540-026-00787-z
UR  - https://doi.org/10.1038/s41540-026-00787-z
AB  - Insufficient sleep is a recognized risk factor for inflammatory diseases, yet how sleep loss functionally perturbs immune regulation remains unclear. Here, we apply a multi-omics framework combining two-sample Mendelian randomization, sleep-restriction intervention microarray, and PBMC single-cell profiling to dissect immune consequences of sleep loss. Mendelian randomization associated genetically proxied sleeplessness/insomnia symptoms with alterations in 162 plasma proteins and increased risk across 94 clinical diagnosis traits. Gene expression microarray after sleep restriction confirmed immune activation and stress-response programs. Single-cell RNA sequencing revealed PBMC remodeling with increased NK/NKT cells and decreased γδ T cells and dendritic cells, alongside pro-inflammatory pathway activity. Ligand–receptor analysis identified altered intercellular communication patterns, characterized by increasing signals to NK cells and enhancing NK–T cell-associated interfaces. These findings nominate dysregulated NK cell–T cell crosstalk as a putative mechanism underlying sleep-related inflammation and provide prioritized targets for future validation.
SN  - 2056-7189
ER  -