| First Author | Swann JB | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 12 | Pages | 7540-9 |
| PubMed ID | 17548588 | Mgi Jnum | J:125812 |
| Mgi Id | MGI:3759951 | Doi | 10.4049/jimmunol.178.12.7540 |
| Citation | Swann JB, et al. (2007) Type I IFN contributes to NK cell homeostasis, activation, and antitumor function. J Immunol 178(12):7540-9 |
| abstractText | This study demonstrates that type I IFNs are an early and critical regulator of NK cell numbers, activation, and antitumor activity. Using both IFNAR1- and IFNAR2-deficient mice, as well as an IFNAR1-blocking Ab, we demonstrate that endogenous type I IFN is critical for controlling NK cell-mediated antitumor responses in many experimental tumor models, including protection from methylcholanthrene-induced sarcomas, resistance to the NK cell-sensitive RMA-S tumor and cytokine immunotherapy of lung metastases. Protection from RMA-S afforded by endogenous type I IFN is more potent than that of other effector molecules such as IFN-gamma, IL-12, IL-18, and perforin. Furthermore, cytokine immunotherapy using IL-12, IL-18, or IL-21 was effective in the absence of endogenous type I IFN, however the antimetastatic activity of IL-2 was abrogated in IFNAR-deficient mice, primarily due to a defect in IL-2-induced cytotoxic activity. This study demonstrates that endogenous type I IFN is a central mediator of NK cell antitumor responses. |
