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in CD8 T Cell-Mediated Elimination of 3LL-A9 Lewis Lung Carcinoma Cells In Vivo1
*
Institute of Medical Microbiology and Hygiene, Department of Immunology, University of Freiburg, Freiburg, Germany; and
Cell Genix Technologie Transfer, GmbH, Freiburg, Germany
The role of perforin, IFN-
, and TNF-
in anti-tumor CD8 T
cell immunity was examined in a new tumor model using a CD8 T cell
epitope (GP33) derived from lymphocytic choriomeningitis virus as a
tumor-associated Ag. In contrast with parental 3LL-A9 (A9) Lewis lung
carcinoma cells that progressively grow in C57BL/6 mice, s.c. injection
of GP33-transfected A9GP33 tumor cells induced a protective
GP33-specific CD8 T cell response that led to complete tumor cell
elimination. Tumor regression was dependent on perforin, IFN-, or
TNF-, because A9GP33 tumors developed in mice deficient
in one of these genes. A9GP33 tumors arising in perforin-
and IFN--deficient mice represented GP33 Ag-loss variants,
demonstrating that GP33-specific CD8 T cells from these mice were able
to exert an Ag selection pressure. In contrast, tumor cells growing in
TNF- knock-out mice still expressed the tumor-associated GP33
peptide despite the presence of activated GP33-specific CD8 T cells.
These findings provide evidence for a crucial role of TNF- in A9
tumor cell elimination by CD8 T cells in vivo.
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