Journal
CANCER RESEARCH
Volume 71, Issue 14, Pages 4790-4798Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-10-1572
Keywords
-
Categories
Funding
- Global Center for Education and Research in Immune System Regulation and Treatment
- MEXT (Japan)
- Ministry of Education, Culture, Sports, Science and Technology (Japan)
- Ministry of Health, Labor and Welfare (Japan) [17016010, 20060003, 21390147, 21591808, 20590485, 205613]
- Uehara Memorial Foundation
- Naito Foundation
- Grants-in-Aid for Scientific Research [21390147, 23659240, 21591808, 23790523, 22591093, 20590485, 17016010, 22300331, 20060003] Funding Source: KAKEN
Ask authors/readers for more resources
Functionally polarized helper T cells (Th cells) play crucial roles in the induction of tumor immunity. There is considerable knowledge about the contributions of IFN-producing Th1 cells that supports the role of cytotoxic cluster of differentiation (CD8) T cells and natural killer (NK) cells, but much less is known about how IL-4-producing Th2 cells contribute to tumor immunity. In this study, we investigated the cellular and molecular mechanisms employed by memory Th2 cells in sustaining tumor immunity by using a mouse model system wherein ovalbumin (OVA) is used as a specific tumor antigen. In this model, we found that OVA-specific memory Th2 cells exerted potent and long-lasting antitumor effects against NK-sensitive OVA-expressing tumor cells, wherein antitumor effects were mediated by NK cells. Specifically, NK cell cytotoxic activity and expression of perforin and granzyme B were dramatically enhanced by the activation of memory Th2 cells. Interleukin 4 (IL-4) produced by memory Th2 cells in vivo was critical for the antitumor effects of the NK cells, which IL-4 directly stimulated to induce their perforin-and granzyme-B-dependent cytotoxic activity. Our findings show that memory Th2 cells can induce potent antitumor immunity through IL-4-induced activation of NK cells, suggesting potential applications in cellular therapy for cancer patients. Cancer Res; 71(14); 4790-8. (C) 2011 AACR.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available