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<p>Hypertrophied adenoids in children can impair breathing and lead to obstructive sleep apnea (OSA), often accompanied by abnormal growth and weakened stamina and immunity. However, the cause of the pathological transformation in these originally immune-enhancing lymphoid tissues remains unclear. Our study provides the first single cell transcriptomic and immune repertoire atlas of adenoids from normal snoring to mild, moderate, and severe OSA, and identified markedly asynchronous functional modules, transcriptional regulatory networks and intercellular communications during the progression of OSA. Children with severe OSA exhibited exhibit active Hippo, Notch, and Wnt signaling, alongside significant downregulation of energy synthesis. Analysis revealed compromised T-cell and B-cell immunity, as well as reduced antigen processing by innate immune cells, coupled with diminished cell-cell communication in severe OSA group. T-cell receptor and B-cell receptor sequencing results also support more infection imprints and abnormal germinal centers and antibody class switching. Mechanistically, HIF1A-mediated hypoxic signaling likely drives the downregulation of key immune components (including HLA and interferon molecules), positioning it as a promising therapeutic target for OSA.</p>

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Disease-stage-specific immunometabolic remodeling in pediatric obstructive sleep apnea: a single-cell transcriptomic atlas of adenoid tissue

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月27日

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  • Qin Yang,
  • Yunfei Cui,
  • Xiao Huang,
  • Junlin Liu,
  • Xiaopeng Ma,
  • George Fu Gao,
  • Hongguang Pan,
  • Shijie Qin

摘要

Hypertrophied adenoids in children can impair breathing and lead to obstructive sleep apnea (OSA), often accompanied by abnormal growth and weakened stamina and immunity. However, the cause of the pathological transformation in these originally immune-enhancing lymphoid tissues remains unclear. Our study provides the first single cell transcriptomic and immune repertoire atlas of adenoids from normal snoring to mild, moderate, and severe OSA, and identified markedly asynchronous functional modules, transcriptional regulatory networks and intercellular communications during the progression of OSA. Children with severe OSA exhibited exhibit active Hippo, Notch, and Wnt signaling, alongside significant downregulation of energy synthesis. Analysis revealed compromised T-cell and B-cell immunity, as well as reduced antigen processing by innate immune cells, coupled with diminished cell-cell communication in severe OSA group. T-cell receptor and B-cell receptor sequencing results also support more infection imprints and abnormal germinal centers and antibody class switching. Mechanistically, HIF1A-mediated hypoxic signaling likely drives the downregulation of key immune components (including HLA and interferon molecules), positioning it as a promising therapeutic target for OSA.