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*
Department of Oncology and Surgical Sciences, Oncology Section, Padova, Italy;
Experimental Immunology Branch, National Cancer Institute-National Institutes of Health, Bethesda, MD 20892; and
Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702
We described a generalized suppression of CTL anamnestic responses
that occurred in mice bearing large tumor nodules or immunized with
powerful recombinant viral immunogens. Immune suppression entirely
depended on GM-CSF-driven accumulation of
CD11b+/Gr-1+ myeloid suppressor cells (MSC) in
secondary lymphoid organs. To further investigate the nature and
properties of MSC, we immortalized CD11b+/Gr-1+
cells isolated from the spleens of immunosuppressed mice, using a
retrovirus encoding the v-myc and v-raf
oncogenes. Immortalized cells expressed monocyte/macrophage markers
(CD11b, F4/80, CD86, CD11c), but they differed from previously
characterized macrophage lines in their capacities to inhibit T
lymphocyte activation. Two MSC lines, MSC-1 and MSC-2, were selected
based upon their abilities to inhibit Ag-specific proliferative and
functional CTL responses. MSC-1 line was constitutively inhibitory,
while suppressive functions of MSC-2 line were stimulated by exposure
to the cytokine IL-4. Both MSC lines triggered the apoptotic cascade in
Ag-activated T lymphocytes by a mechanism requiring cell-cell contact.
Some well-known membrane molecules involved in the activation of
apoptotic pathways (e.g., TNF-related apoptosis-inducing ligand, Fas
ligand, TNF-
) were ruled out as candidate effectors for the
suppression mechanism. The immortalized myeloid lines represent a
novel, useful tool to shed light on the molecules involved in the
differentiation of myeloid-related suppressors as well as in the
inhibitory pathway they use to control T lymphocyte
activation.
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