The Journal of Experimental Medicine
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Published online 29 August 2005 doi:10.1084/jem.20050994
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 5, 583-588
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BRIEF DEFINITIVE REPORT

 NKG2D function protects the host from tumor initiation

Mark J. Smyth1, Jeremy Swann1, Erika Cretney1, Nadeen Zerafa1, Wayne M. Yokoyama2, and Yoshihiro Hayakawa1

1 Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, East Melbourne, Victoria 3002, Australia
2 Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, MO 63110

CORRESPONDENCE Mark Smyth: mark.smyth{at}petermac.org

The activation NKG2D receptor has been shown to play an important role in the control of experimental tumor growth and metastases expressing ligands for NKG2D; however, a function for this recognition pathway in host protection from de novo tumorigenesis has never been demonstrated. We show that neutralization of NKG2D enhances the sensitivity of wild-type (WT) C57BL/6 and BALB/c mice to methylcholanthrene (MCA)-induced fibrosarcoma. The importance of the NKG2D pathway was additionally illustrated in mice deficient for either IFN-{gamma} or tumor necrosis factor–related apoptosis-inducing ligand, whereas mice depleted of natural killer cells, T cells, or deficient for perforin did not display any detectable NKG2D phenotype. Furthermore, IL-12 therapy preventing MCA-induced sarcoma formation was also largely dependent on the NKG2D pathway. Although NKG2D ligand expression was variable or absent on sarcomas emerging in WT mice, sarcomas derived from perforin-deficient mice were Rae-1+ and immunogenic when transferred into WT syngeneic mice. These findings suggest an important early role for the NKG2D in controlling and shaping tumor formation.


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