scRNA-seq of gastric tumor shows complex intercellular interaction with an alternative T cell exhaustion trajectory

Keyong Sun, Runda Xu, Fuhai Ma, Naixue Yang, Yang Li, Xiaofeng Sun, Peng Jin, Wenzhe Kang, Lemei Jia, Jianping Xiong, Haitao Hu, Yantao Tian () and Xun Lan ()
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Keyong Sun: Tsinghua University
Runda Xu: Tsinghua University
Fuhai Ma: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Naixue Yang: Tsinghua University
Yang Li: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Xiaofeng Sun: Tsinghua University
Peng Jin: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Wenzhe Kang: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Lemei Jia: Tsinghua University
Jianping Xiong: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Haitao Hu: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Yantao Tian: Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Nanli
Xun Lan: Tsinghua University

Nature Communications, 2022, vol. 13, issue 1, 1-19

Abstract: Abstract The tumor microenvironment (TME) in gastric cancer (GC) has been shown to be important for tumor control but the specific characteristics for GC are not fully appreciated. We generated an atlas of 166,533 cells from 10 GC patients with matched paratumor tissues and blood. Our results show tumor-associated stromal cells (TASCs) have upregulated activity of Wnt signaling and angiogenesis, and are negatively correlated with survival. Tumor-associated macrophages and LAMP3+ DCs are involved in mediating T cell activity and form intercellular interaction hubs with TASCs. Clonotype and trajectory analysis demonstrates that Tc17 (IL-17+CD8+ T cells) originate from tissue-resident memory T cells and can subsequently differentiate into exhausted T cells, suggesting an alternative pathway for T cell exhaustion. Our results indicate that IL17+ cells may promote tumor progression through IL17, IL22, and IL26 signaling, highlighting the possibility of targeting IL17+ cells and associated signaling pathways as a therapeutic strategy to treat GC.

Date: 2022
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DOI: 10.1038/s41467-022-32627-z

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