Abstract
Luciferase-transduced B16 murine melanoma cells (luc-B16) inoculated in ear skin do not form tumors but prevent tumor formation by luc-B16 cells injected into the footpad. To determine the requirements for such immunity, we followed the fate of luc-B16 cells following ear injection. Surprisingly, small numbers of viable luc-B16 cells were detected in tumor-free mouse skin for up to 60 days post-inoculation. After 1 week, the number of Foxp3+CD4 +CD25+ T cells (along with foxp3 mRNA expression) increased rapidly in the injected ear skin. Residual tumor cells in ears were reduced in mice treated with anti-CD25 mAb and in CD4-deficient mice, but increased in CD8-deficient mice. Strikingly, the loss of luc-B16 cells in the ear skin, either spontaneously or following amputation of the injected ear, resulted in significantly enhanced tumor formation by parental and luciferase-expressing B16 cells after footpad injection. These studies suggest that small numbers of tumor cells (possibly regulated by CD4 +CD25+ regulatory T cells expressing Foxp3) are required for effective host anti-tumor responses at alternate inoculation sites.
Original language | English (US) |
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Pages (from-to) | 1119-1131 |
Number of pages | 13 |
Journal | Cancer Immunology, Immunotherapy |
Volume | 56 |
Issue number | 7 |
DOIs | |
State | Published - Jul 2007 |
Externally published | Yes |
Keywords
- CD4
- Regulatory T cells
- Tumorigenesis
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Oncology
- Cancer Research