Immune effector monocyte–neutrophil cooperation induced by the primary tumor prevents metastatic progression of breast cancer

Research output: Contribution to journalArticle


Metastatic behavior varies significantly among breast cancers. Mechanisms explaining why the majority of breast cancer patients never develop metastatic outgrowth are largely lacking but could underlie the development of novel immunotherapeutic target molecules. Here we show interplay between nonmetastatic primary breast cancer and innate immune response, acting together to control metastatic progression. The primary tumor systemically recruits IFNγ-producing immune effector monocytes to the lung. IFNγ up-regulates Tmem173/ STING in neutrophils and enhances their killing capacity. The immune effector monocytes and tumoricidal neutrophils target disseminated tumor cells in the lungs, preventing metastatic outgrowth. Importantly, our findings could underlie the development of immunotherapeutic target molecules that augment the function of immune effector monocytes and neutrophils.


External organisations
  • University of California, San Francisco
  • UCSF Helen Diller Family Comprehensive Cancer Center
  • Skåne University Hospital
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Cancer and Oncology


  • CCL2, CCR2, Immune effector monocytes, Metastatic breast cancer, STING
Original languageEnglish
Pages (from-to)21704-21714
Number of pages11
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number43
Publication statusPublished - 2019
Publication categoryResearch