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<p>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.</p>

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Sleep restriction reprograms systemic immunity through NK and T cell crosstalk

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月14日

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  • Zhengyang Qiu,
  • Jichen Jin,
  • Pengqi Zhang,
  • Chen Li,
  • Yongmei Xi

摘要

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.