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CUTTING EDGE |
Department of Pathology and Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL 60637
Several lines of evidence suggest that an IFN-
-producing,
Th1/Tc1 phenotype may be optimal for tumor rejection. Recent work has
indicated that IFN signaling on tumor cells is important for protection
against carcinogenesis. However, the potential involvement of IFN
signaling among host immune cells has not been carefully examined. To
this end, Stat1-deficient mice were employed as tumor recipients. In
contrast to wild-type mice, Stat1-/- mice failed to
reject immunogenic tumors and did not support regression of poorly
immunogenic tumors when treated with an IL-12-based vaccine. T cells
from immunized Stat1-/- mice produced 50% of the levels
of IFN- and lacked cytolytic activity compared with wild-type mice,
and NK lytic activity also was not observed. Lack of cytolytic function
correlated with a failure to up-regulate serine esterase activity.
Thus, IFN-mediated signaling on host cells is required for the
development of antitumor lytic effector cells.
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