Patrolling monocytes control tumor metastasis to the lung
Author(s)
Date
2015Source Title
Science
Print ISSN
0036-8075
Publisher
American Association for the Advancement of Science
Volume
350
Issue
6263
Pages
985 - 990
Language
English
Type
ArticleItem Usage Stats
139
views
views
108
downloads
downloads
Abstract
The immune system plays an important role in regulating tumor growth and metastasis. Classical monocytes promote tumorigenesis and cancer metastasis, but how nonclassical "patrolling" monocytes (PMo) interact with tumors is unknown. Here we show that PMo are enriched in the microvasculature of the lung and reduce tumor metastasis to lung in multiple mouse metastatic tumor models. Nr4a1-deficient mice, which specifically lack PMo, showed increased lung metastasis in vivo. Transfer of Nr4a1-proficient PMo into Nr4a1-deficient mice prevented tumor invasion in the lung. PMo established early interactions with metastasizing tumor cells, scavenged tumor material from the lung vasculature, and promoted natural killer cell recruitment and activation. Thus, PMo contribute to cancer immunosurveillance and may be targets for cancer immunotherapy.
Keywords
AnatomyBlood
Cancer
Cells and cell components
Disease treatment
Immune system
Respiratory disease
Rodent
Tumor
Animal cell
Animal experiment
Animal model
Article
Cancer control
Cell interaction
Cell specificity
Cell transfer
Controlled study
Female
In vivo study
Lung metastasis
Microvasculature
Monocyte
Mouse
Natural killer cell
Nonhuman
Priority journal
Tumor cell
Tumor invasion
Animal
Experimental neoplasm
Genetics
Immunology
Immunosurveillance
Immunotherapy
Lung Neoplasms
Metastasis
Monocyte
Mutant mouse strain
Procedures
Secondary
Mus
Nr4a1 protein, mouse
Nuclear receptor Nur77
Animals
Immunologic Surveillance
Immunotherapy
Killer Cells, Natural
Lung Neoplasms
Mice
Mice, Mutant Strains
Monocytes
Neoplasm Invasiveness
Neoplasm Metastasis
Neoplasms, Experimental
Nuclear Receptor Subfamily 4, Group A, Member 1
Permalink
http://hdl.handle.net/11693/26419Published Version (Please cite this version)
http://dx.doi.org/10.1126/science.aac9407Collections
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