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<p><i>Helicobacter pylori</i> (<i>H. pylori</i>) manipulates the host immune system to establish a persistent colonization, posing a serious threat to human health, but the mechanisms remain poorly understood. Here we integrate single-cell RNA sequencing and TCR profiling for analyzing 187,192 cells from 11 <i>H. pylori</i>-negative and 12 <i>H. pylori</i>-positive individuals to describe the human gastric ecosystem reprogrammed by <i>H. pylori</i> infection, as manifested by impaired antigen presentation and phagocytosis function. We further delineate a monocyte-to-C1QC<sup>+</sup> macrophage differentiation trajectory driven by <i>H. pylori</i> infection, while T cell responses exhibit broad functional impairment and hyporesponsiveness with restricted clonal expansion capacity. We also identify an HLA-DRs- and CTLA4-expressing T cell population residing in <i>H. pylori</i>-inhabited stomach that potentially contribute to immune evasion. Together, our findings provide single-cell resolution information into the immunosuppressive microenvironment shaped by <i>H. pylori</i> infection, offering critical insights for developing novel therapeutic approaches to eliminate this globally prevalent pathogen.</p>

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Single-cell RNA sequencing dissects the immunosuppressive signatures in Helicobacter pylori-infected human gastric ecosystem

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月25日

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  • Wei Hu,
  • Ze Min Chen,
  • Ying Wang,
  • Chao Yang,
  • Zi Ying Wu,
  • Li Juan You,
  • Zhi Yong Zhai,
  • Zhao Yu Huang,
  • Ping Zhou,
  • Si Lin Huang,
  • Xia Xi Li,
  • Gen Hua Yang,
  • Chong Ju Bao,
  • Xiao Bing Cui,
  • Gui Li Xia,
  • Mei Ping Ou Yang,
  • Lin Zhang,
  • William Ka Kei Wu,
  • Long Fei Li,
  • Li Kai Tan,
  • Yu Xuan Zhang,
  • Wei Gong

摘要

Helicobacter pylori (H. pylori) manipulates the host immune system to establish a persistent colonization, posing a serious threat to human health, but the mechanisms remain poorly understood. Here we integrate single-cell RNA sequencing and TCR profiling for analyzing 187,192 cells from 11 H. pylori-negative and 12 H. pylori-positive individuals to describe the human gastric ecosystem reprogrammed by H. pylori infection, as manifested by impaired antigen presentation and phagocytosis function. We further delineate a monocyte-to-C1QC+ macrophage differentiation trajectory driven by H. pylori infection, while T cell responses exhibit broad functional impairment and hyporesponsiveness with restricted clonal expansion capacity. We also identify an HLA-DRs- and CTLA4-expressing T cell population residing in H. pylori-inhabited stomach that potentially contribute to immune evasion. Together, our findings provide single-cell resolution information into the immunosuppressive microenvironment shaped by H. pylori infection, offering critical insights for developing novel therapeutic approaches to eliminate this globally prevalent pathogen.