| First Author | Smyth MJ | Year | 2005 |
| Journal | J Exp Med | Volume | 202 |
| Issue | 5 | Pages | 583-8 |
| PubMed ID | 16129707 | Mgi Jnum | J:100684 |
| Mgi Id | MGI:3589303 | Doi | 10.1084/jem.20050994 |
| Citation | Smyth MJ, et al. (2005) NKG2D function protects the host from tumor initiation. J Exp Med 202(5):583-8 |
| abstractText | 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. |
