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* Laboratory of Molecular and Tumor Immunology, Robert W. Franz Cancer Research Center, Earle A. Chiles Research Institute, Providence Cancer Center and Providence Portland Medical Center, Portland, OR 97213; Departments of
Biochemistry and Molecular Biology and
Molecular Microbiology and Immunology, and
Oregon Cancer Center, Oregon Health and Science University, Portland, OR 97201;
¶ Institute of Immunopathology, School of Life Science, Xi’an Jiaotong University, Xi’an, China; and
|| Department of Immunochemistry, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121
Previously, we have shown that priming of therapeutic
CD8+ T cells in tumor vaccine-draining lymph nodes of mice
vaccinated with GM-CSF secreting B16BL6 melanoma cells occurs
independent of CD4 T cell help. In this study, we examined the
contribution of the major costimulatory molecules, CD40 ligand (CD40L),
CD80, and CD86, in the priming of CD8+ T cells. Priming of
therapeutic CD8+ T cells by a GM-CSF-transduced tumor
vaccine did not require CD40 and CD40L interactions, as therapeutic T
cells could be generated from mice injected with anti-CD40L Ab and
from CD40L knockout mice. However, costimulation via either CD80 or
CD86 was required, as therapeutic T cells could be generated from mice
injected with either anti-CD80 or anti-CD86 Ab alone, but
administration of both Abs completely inhibited the priming of
therapeutic T cells. Blocking experiments also identified that
priming of therapeutic T cells in MHC class II-deficient mice required
TNFR and IL-12 signaling, but signaling through CD40, lymphotoxin-
R,
or receptor activator of NF-
B was not essential. Thus,
cross-priming of therapeutic CD8+ T cells by a tumor
vaccine transduced with GM-CSF requires TNFR, IL-12, and CD28
signaling.
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