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*
Department of Cell Biology and Kaplan Cancer Center, New York University School of Medicine, New York, NY 10016;
Second Department of Pathology, Gifu University School of Medicine, Gifu, Japan;
Institute of Molecular Genetics and Genetic Engineering, Belgrade, Yugoslavia; and
Ludwig Institute for Cancer Research, Memorial Sloan-Kettering Cancer Center, New York, NY 10021
We have investigated the ability of different cells present in
murine tumors to induce apoptosis of activated CD8+
T cells in vitro. Tumor cells do not induce apoptosis of T cells;
however, macrophages that infiltrate tumors are potent inducers of
apoptosis. Tumor macrophages express cell surface-associated TNF, TNF
type I (CD120a) and II (CD120b) receptors, and, upon contact with T
cells which induces release of IFN-
from T cells, secrete nitric
oxide. Killing of T cells in vitro is blocked by Abs to IFN-, TNF,
CD120a, or CD120b, or N-methyl-L-arginine.
In concert with that finding, tumor macrophages isolated from either
TNF type I or type II receptor -/- mice are not proapoptotic and do
not produce nitric oxide upon contact with activated T cells. Control
macrophages do not express TNF receptors or release nitric oxide. Tumor
cells or tumor-derived macrophages do not express FasL, and blocking
Abs to either Fas or FasL have no effect on macrophage-mediated T cell
killing. These results demonstrate that macrophages which infiltrate
tumors are highly proapoptotic and may be responsible for elimination
of activated antitumor T cells within the tumor
bed.
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