期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 39, 期 2, 页码 457-468出版社
WILEY
DOI: 10.1002/eji.200838794
关键词
DC; IFN-gamma; NK cells; Tumor immunity; Vaccination
类别
资金
- Ministry of Education, Science, Sports, and Culture of Japan
- Mitsubishi Pharma Research Foundation
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据