Classical inflammatory monocytes and their derivative macrophages promote tumor metastasis whereas CD8+ T and NK cells restrict tumor growth. In a recent paper published in Science, Hanna and colleagues demonstrate that another monocyte population, nonclassical patrolling monocytes, is enriched in the microvasculature of tumor-challenged lung and reduces tumor metastasis by recruiting NK cells.

Tumor metastasis accounts for 95% of cancer-related deaths in the developed world. In the past decade focus has shifted from study of cancer cells alone to the tumor microenvironment that consists of many cell types that overall support cancer progression. Circulating monocytes extravasate into the tissue and differentiate into macrophages, which are key players in the regulation of metastasis as they provide support for the extravasation, survival and growth of metastatic cancer cells [1]. There are at least two circulating monocyte populations in the blood: classical “inflammatory” monocytes (IMo, CCR2HighLy6C+ in mouse; CCR2High CD14++CD16‒in human) and nonclassical “patrolling” monocytes (PMo, CX3CR1HighLy6C‒in mouse; CX3CR1HighCD14+CD16+ in human). IMo are recruited to inflammatory sites through the CCR2-CCL2 axis; they extravasate, differentiate into tissue macrophages and dendritic cells, and respond to bacterial and parasitic infections. In breast cancer models, IMo are also recruited via the CCL2-CCR2 axis to metastatic sites where they promote cancer cell extravasation and survival [2].