| First Author | Shimizu K | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 2 | Pages | 457-68 |
| PubMed ID | 19180466 | Mgi Jnum | J:144471 |
| Mgi Id | MGI:3831014 | Doi | 10.1002/eji.200838794 |
| Citation | Shimizu K, et al. (2009) DC therapy induces long-term NK reactivity to tumors via host DC. Eur J Immunol 39(2):457-68 |
| abstractText | We vaccinated mice with DC loaded with or without invariant NKT-cell ligand alpha-galactosylceramide and evaluated long-term resistance against tumor challenge. When mice had been given either DC or DC/galactosylceramide and were challenged with tumor cells even 6-12 months later, both NK and NKT cells were quickly activated to express CD69 and produce IFN-gamma. The NK cells could resist a challenge with several different tumors in vivo. The activated NK and NKT cells could be depleted with anti-NK1.1 treatment. In spite of this, the activated cells recovered, indicating that tumor-responsive NK and NKT cells were being generated continuously as a result of vaccination with DC and were not true memory cells. The NK and NKT antitumor response in DC-vaccinated mice depended on CD4(+) T cells, but neither CD8(+)T cells nor CD4(+)CD25(+) regulatory T cells. However, both vaccine DC and host DC were required for the development of long-term, tumor reactive innate immunity. These results indicate that DC therapy in mice induces long-lasting innate NK- and NKT-cell activation through a pathway that requires host DC and CD4(+) T cells and that the continued generation of active NK cells resists the establishment of metastases in vivo. |
