Small numbers of residual tumor cells at the site of primary inoculation are critical for anti-tumor immunity following challenge at a secondary location |
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Authors: | Takashi Kakinuma Hari Nadiminti Anke S Lonsdorf Takashi Murakami Bradford A Perez Hisataka Kobayashi Steven E Finkelstein Gulnar Pothiawala Yasmine Belkaid Sam T Hwang |
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Institution: | (1) Laboratory of Parasitic Diseases, NIAID, Bethesda, MD 20892, USA;(2) Metabolism Branch, Center for Cancer Research, NCI, Bethesda, MD 20892, USA;(3) Surgery Branch, Center for Cancer Research, NCI, Bethesda, MD 20892, USA;(4) Dermatology Branch, Center for Cancer Research, NCI, Bldg 10/Rm12N246, 10 Center Dr., Bethesda, MD 20892-1908, USA |
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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. |
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Keywords: | Tumorigenesis Regulatory T cells CD4 |
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