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CCL7 recruits cDC1 to promote antitumor immunity and facilitate checkpoint immunotherapy to non-small cell lung cancer

Author

Listed:
  • Man Zhang

    (Medical Research Institute, Zhongnan Hospital of Wuhan University
    Wuhan University
    Wuhan University)

  • Wei Yang

    (Medical Research Institute, Zhongnan Hospital of Wuhan University
    Wuhan University
    Wuhan University)

  • Peng Wang

    (Medical Research Institute, Zhongnan Hospital of Wuhan University
    Wuhan University
    Wuhan University)

  • Yu Deng

    (Tongji Medical College, Huazhong University of Science and Technology)

  • Yu-Ting Dong

    (Huazhong University of Science and Technology
    Huazhong University of Science and Technology)

  • Fang-Fang Liu

    (Tongji Medical College, Huazhong University of Science and Technology)

  • Rui Huang

    (Third Military Medical University (Army Medical University))

  • Peng Zhang

    (Tongji Medical College, Huazhong University of Science and Technology)

  • Ya-Qi Duan

    (Huazhong University of Science and Technology
    Huazhong University of Science and Technology)

  • Xin-Dong Liu

    (Third Military Medical University (Army Medical University))

  • Dandan Lin

    (Cancer Center, Renmin Hospital of Wuhan University)

  • Qian Chu

    (Tongji Medical College, Huazhong University of Science and Technology)

  • Bo Zhong

    (Medical Research Institute, Zhongnan Hospital of Wuhan University
    Wuhan University
    Wuhan University)

Abstract

The efficacy of checkpoint immunotherapy to non-small cell lung cancer (NSCLC) largely depends on the tumor microenvironment (TME). Here, we demonstrate that CCL7 facilitates anti-PD-1 therapy for the KrasLSL−G12D/+Tp53fl/fl (KP) and the KrasLSL−G12D/+Lkb1fl/fl (KL) NSCLC mouse models by recruiting conventional DC 1 (cDC1) into the TME to promote T cell expansion. CCL7 exhibits high expression in NSCLC tumor tissues and is positively correlated with the infiltration of cDC1 in the TME and the overall survival of NSCLC patients. CCL7 deficiency impairs the infiltration of cDC1 in the TME and the subsequent expansion of CD8+ and CD4+ T cells in bronchial draining lymph nodes and TME, thereby promoting tumor development in the KP mouse model. Administration of CCL7 into lungs alone or in combination with anti-PD-1 significantly inhibits tumor development and prolongs the survival of KP and KL mice. These findings suggest that CCL7 potentially serves as a biomarker and adjuvant for checkpoint immunotherapy of NSCLC.

Suggested Citation

  • Man Zhang & Wei Yang & Peng Wang & Yu Deng & Yu-Ting Dong & Fang-Fang Liu & Rui Huang & Peng Zhang & Ya-Qi Duan & Xin-Dong Liu & Dandan Lin & Qian Chu & Bo Zhong, 2020. "CCL7 recruits cDC1 to promote antitumor immunity and facilitate checkpoint immunotherapy to non-small cell lung cancer," Nature Communications, Nature, vol. 11(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19973-6
    DOI: 10.1038/s41467-020-19973-6
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    Cited by:

    1. Wenjun Xiong & Xueliang Gao & Tiantian Zhang & Baishan Jiang & Ming-Ming Hu & Xia Bu & Yang Gao & Lin-Zhou Zhang & Bo-Lin Xiao & Chuan He & Yishuang Sun & Haiou Li & Jie Shi & Xiangling Xiao & Bolin X, 2022. "USP8 inhibition reshapes an inflamed tumor microenvironment that potentiates the immunotherapy," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    2. Andre Lima Queiroz & Ezequiel Dantas & Shakti Ramsamooj & Anirudh Murthy & Mujmmail Ahmed & Elizabeth R. M. Zunica & Roger J. Liang & Jessica Murphy & Corey D. Holman & Curtis J. Bare & Gregory Ghahra, 2022. "Blocking ActRIIB and restoring appetite reverses cachexia and improves survival in mice with lung cancer," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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