Tumor initiating cells escape tumor immunity via CCL8 from tumor-associated macrophages in mice.

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Tác giả: Demeng Chen, Shuang Chen, Maosheng Cheng, Chen-Song Huang, Heping Li, Kang Li, Rongsong Ling, Jieyi Ma, Liang Peng, Zhenwei Peng, Guoli Tian, Xiaochen Wang, Gan Xiong, Jianqi Xiong, Caihua Zhang, Zhihui Zhang, Bin Zhou, Ruoxing Zhou, Yan Zhu

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: United States : The Journal of clinical investigation , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 730200

Tumor-initiating cells (TICs) play a key role in cancer progression and immune escape. However, how TICs evade immune elimination remains poorly characterized. Combining single-cell RNA sequencing (scRNA-seq), dual-recombinase-based lineage tracing, and other approaches, we identified a WNT-activated subpopulation of malignant cells that act as TICs in vivo. We found intensive reciprocal interactions between TICs and immune regulatory tumor-associated macrophages (Reg-TAMs) via GAS6-AXL/MERTK signaling pathways, which facilitated the immune escape of TICs. Our study employed chemical inhibitors and Axl/Mertk conditional double knockout mice to demonstrate that inhibiting the interaction between TIC-derived GAS6 and AXL/MERTK in Reg-TAMs reactivated anti-tumor immune responses. We identified CCL8 as a critical mediator of the GAS6/AXL/MERTK pathway, primarily by inhibiting regulatory T cell (Treg) infiltration into the tumor. Furthermore, the AXL/MERTK signaling blockade sensitized tumor cells to anti-PD-1 treatment. Thus, we elucidated a detailed mechanism by which TICs evade tumor immunity, providing insights into strategies to eradicate TICs that escape conventional immunotherapy.
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