Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 116, Issue 43, Pages 21704-21714Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1907660116
Keywords
metastatic breast cancer; immune effector monocytes; CCR2; CCL2; STING
Categories
Funding
- National Cancer Institute [CA057621, CA180039, CA199315, CA190851]
- Parker Institute for Immunotherapy
- Tegger Foundation
- Wenner-Gren Foundations
- Sweden-America Foundation
- Swedish Society of Medicine
- Lakaresallskapet i Lund
- Swedish Society for Medical Research
- Becas Chile Scholarship
- Taiwan Ministry of Science and Technology [MOST104-2917-I-006-002]
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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 IFN gamma-producing immune effector monocytes to the lung. IFN gamma 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.
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