2. Academic Validation
  3. CD169+ macrophages identify and eliminate tumor cells in colorectal cancer through CD169/CD43 interaction and FasL-driven apoptosis

CD169+ macrophages identify and eliminate tumor cells in colorectal cancer through CD169/CD43 interaction and FasL-driven apoptosis

  • Cell Rep. 2025 Sep 26;44(10):116351. doi: 10.1016/j.celrep.2025.116351.
Junqing Hu 1,  Feilong Guo 2,  Congwei Han 3,  Qiqi Zhao 3,  Huaiqiang Yi 3,  Jinhao Xu 3,  Huijie Jia 3,  Yongjie Wu 3,  Lei Dong 3,  Xiaoming Kao 2,  Guoli Li 4,  Jiangning Chen 5,  Junfeng Zhang 6,  Zhen Huang 7
Affiliations

Affiliations

  • 1 State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China; NJU Xishan Institute of Applied Biotechnology, Xishan District, Wuxi, Jiangsu 214101, China.
  • 2 Department of General Surgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, China.
  • 3 State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China.
  • 4 Department of General Surgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu 210002, China. Electronic address: liguoli@csco.org.cn.
  • 5 State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China; State Key Laboratory of Analytical Chemistry for Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China. Electronic address: jnchen@nju.edu.cn.
  • 6 State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China. Electronic address: jfzhang@nju.edu.cn.
  • 7 State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China; NJU Xishan Institute of Applied Biotechnology, Xishan District, Wuxi, Jiangsu 214101, China. Electronic address: zhenhuang@nju.edu.cn.
PMID: 41016034 DOI: 10.1016/j.celrep.2025.116351
Abstract

Tumor-associated macrophages (TAMs) play key roles in tumor progression and therapy resistance. In colorectal Cancer (CRC), TAM heterogeneity challenges macrophage-targeted therapies, with certain antitumor macrophage subpopulations not yet fully characterized. This study bridges this gap by identifying a distinct subset of tumoricidal CD169+ macrophages. Increased infiltration of CD169+ macrophages was observed in CRC tissues, which was significantly associated with improved overall survival in patients with CRC. Deleting CD169+ macrophages in genetically engineered mouse models (MC38 orthotopic/ectopic and CD169DTR/+APCMin/+ intestinal adenoma) accelerated tumor growth. Integrated multi-omics data and functional assays, including cell coculture models and animal experiments with antibody blockade, reveal an antitumor mechanism in which CD169+ macrophages directly interact with CRC cells. This interaction, mediated by CD169/CD43 molecular engagements, leads to tumor cell Apoptosis via high levels of factor-related Apoptosis ligand (FasL). Our results not only deepen our understanding of the CRC tumor microenvironment but also open avenues for Cancer Immunotherapy targeting.

Keywords

CD169(+) macrophages; CD43; CP: Cancer; CP: Immunology; FasL; colorectal cancer.

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