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*
Division of Neurosurgery and
Department of Anatomy, Virginia Commonwealth University/Medical College of Virginia, Richmond, VA 23198
Previously, we reported that IL-6 transduction attenuates tumor
formation of a rat T9 glioma clone (termed T9.F). This study focuses on
the mechanisms of the antitumor response elicited by IL-6 and the
generation of glioma immunity. Ten days post s.c. inoculation of T9.F-
or IL-6-secreting T9.F cells (T9.F/IL6/hi), tumor nodules were removed
and their leukocytic infiltrate was analyzed by FACS with Ab markers
for T cells, B cells, granulocytes, and monocytes. T9.F/IL6/hi tumors
showed a marked increase in granulocytes as compared with parental T9.F
tumors, and histological examination revealed that the granulocytes
were neutrophils. Animals made neutropenic failed to reject T9.F/IL6/hi
tumors. FACS analysis of 17-day T9.F/IL6/hi regressing tumors and T9.F
progressing tumors did not reveal any significant differences in the
leukocytic infiltrates. Tumor-specific effector cells were detected in
the spleens harvested from animals bearing 17-day, regressing,
T9.F/IL6/hi tumors. In vitro, these effector cells lysed T9.F cells,
proliferated in response to T9.F stimulator cells, and produced Th1
cytokines (IL-2 and IFN-
) but not the Th2 cytokine, IL-4, when
cocultured with T9.F stimulator cells. Rats that had rejected s.c.
T9.F/IL6/hi tumors displayed a delayed-type hypersensitivity response
when injected with viable T9.F cells in the contralateral flank.
Passive transfer of spleen cells from these animals transferred glioma
immunity to naive recipients and depletion of CD3+ T cells,
before transfer, completely abolished immunity, whereas depletion of
CD8+ T cells had moderate inhibitory effects on the
transfer of immunity.
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