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Updated: Jun 25, 2026

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model
Published on: April 13, 2015
Natural killer cells require selectins for suppression of subcutaneous tumors
Olga Sobolev1, Patrick Stern, Adam Lacy-Hulbert
1Howard Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Abstract:
Natural killer (NK) cells recognize and destroy cancer cells through a variety of mechanisms. They may also modulate the adaptive immune response to cancer by interacting with dendritic cells and T cells. Although NK cells play an important role in tumor suppression, little is known about the mechanisms of their recruitment to tumors. Previously it has been shown that subcutaneous tumor growth is enhanced in mice lacking selectins, a family of cell adhesion molecules that mediate the first step of immune cell entry into tissue from the blood. Here we show that NK cell recruitment to tumors is defective in selectin-deficient mice. In vivo NK cell depletion, either pharmacologic or genetic, leads to enhanced subcutaneous tumor growth, similar to the phenotype observed in the selectin-deficient animals. We also show that although NK cells from selectin-deficient mice appear developmentally normal and are functional in in vitro assays, their in vivo function is impaired. This study reveals a role for selectins in NK cell recruitment to tumors and in regulation of effective tumor immunity.
Insights
Selectins are crucial for recruiting natural killer (NK) cells to tumors. Defective selectin function impairs NK cell anti-cancer activity, leading to enhanced tumor growth.
Area of Science:
- Immunology
- Cancer Biology
- Cellular Adhesion
Background:
- Natural killer (NK) cells are vital for tumor suppression, but their recruitment mechanisms to tumor sites remain unclear.
- Selectins, a family of cell adhesion molecules, are known to mediate initial immune cell trafficking into tissues.
- Previous studies indicated enhanced tumor growth in mice lacking selectins.
Purpose of the Study:
- To investigate the role of selectins in the recruitment of NK cells to tumors.
- To determine the impact of selectin deficiency on NK cell function in vivo.
- To elucidate the contribution of NK cells to tumor immunity regulation.
Main Methods:
- Utilizing selectin-deficient mice models.
- Employing in vivo NK cell depletion (pharmacologic and genetic).
- Assessing NK cell recruitment, development, and in vitro/in vivo function.
Main Results:
- NK cell recruitment to tumors was significantly impaired in selectin-deficient mice.
- In vivo depletion of NK cells mimicked the enhanced tumor growth phenotype seen in selectin-deficient animals.
- NK cells from selectin-deficient mice showed normal development and in vitro function but impaired in vivo activity.
Conclusions:
- Selectins play a critical role in facilitating NK cell infiltration into tumors.
- Impaired NK cell recruitment due to selectin deficiency compromises anti-tumor immunity.
- Selectins are essential regulators of NK cell-mediated tumor surveillance and control.
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