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CUTTING EDGE |
*
Department of Pathology and the Committee on Immunology, and
Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL 60637
Experimental evidence suggests that a type 1 T cell response may
result in optimal tumor rejection in vivo. This phenotype is determined
in part by cytokines that influence T cell differentiation. In
transplantable tumor models such as P1.HTR, tumors grow progressively
despite expression of defined tumor Ags. We hypothesized that this
failure to reject may be due to poor generation of a type 1 phenotype,
through a dominant influence of the type 2-promoting cytokines IL-4
and/or IL-13. This hypothesis was tested by implanting P1.HTR tumors
into mice deficient in Stat6. In contrast to progressive growth of
P1.HTR tumors in wild-type mice, and aggressive growth even of
IL-12-transfected P1.HTR in Stat1-/- mice, P1.HTR was
spontaneously rejected by Stat6-/- mice. Rejection was
accompanied by augmented tumor-specific IFN-
production and CTL
activity. These results suggest that pharmacologic inhibition of Stat6
signaling could potentiate anti-tumor immunity in
vivo.
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