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* Institute of Medical Microbiology and Hygiene, Department of Immunology, University of Freiburg, Freiburg, Germany;
Institute of Experimental Immunology, University Hospital, Zurich, Switzerland; and
Cell Genix Technologie Transfer GmbH, Freiburg, Germany
Tumor-specific CD8 T cell responses to MCA102 fibrosarcoma cells
expressing the cytotoxic T cell epitope gp33 from lymphocytic
choriomeningitis virus were studied. MCA102gp33 tumors grew
progressively in C57BL/6 mice, despite induction of peripheral
gp33-tetramer+ T cells that were capable of mediating
antiviral protection, specific cell rejection, and concomitant tumor
immunity. MCA102gp33 tumors were infiltrated with a high
number (
20%) of CD11b+CD11c-
macrophage-phenotype cells that were able to cross-present the gp33
epitope to T cells. Tumor-infiltrating CD8 T cells exhibited a highly
activated phenotype but lacked effector cell function. Strikingly, a
significant portion of tumor-infiltrating lymphocytes expressed TCRs
specific for gp33 but bound MHC tetramers only after cell purification
and a 24-h resting period in vitro. The phenomenon of
"tetramer-negative T cells" was not restricted to
tumor-infiltrating lymphocytes from MCA102gp33 tumors, but
was also observed when Ag-specific T cells derived from an environment
with high Ag load were analyzed ex vivo. Thus, using a novel tumor
model, allowing us to trace tumor-specific T cells at the single cell
level in vivo, we demonstrate that the tumor microenvironment is able
to alter the functional activity of T cells infiltrating the tumor
mass.
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