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Human Tumor Immunobiology and
Human Tumor Immunotherapy Units, Department of Experimental Oncology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy
In this study we tested the hypothesis that loss of T cell
signaling molecules in metastatic melanoma patients’ T cells may
affect differently T cell subsets characterized by distinct TCR
variable regions. By a two-color immunofluorescence technique,
expression of 
-chain, lck, and ZAP-70 was evaluated
in CD3+ T cells and in three representative T cell subsets
expressing TCRAV2, TCRBV2, or TCRBV18. Partial loss of
lck and ZAP-70 was found in CD3+ T cells
from PBL of most melanoma patients, but not of healthy donors. The
extent of -chain, lck, and ZAP-70 loss depended on
the TCRV region expressed by the T cells, and this association was
maintained or increased during progression of disease. Coculture of
patients’ or donors’ T cell with melanoma cells, or with their
supernatants, but not with normal fibroblasts or their supernatants,
down-modulated expression of -chain, lck, and ZAP-70
in a TCRV region-dependent way. Immunodepletion of soluble HLA class I
molecules present in tumor supernatants, but not of soluble ICAM-1,
blocked the suppressive effect on T cell signaling molecule expression.
T cell activation with mAbs to a single TCRV region and to CD28 led to
significant and TCRV region-specific re-induction of -chain
expression. These findings indicate that extent of TCR signaling
molecules loss in T lymphocytes from metastatic melanoma patients
depends on the TCRV region and suggest that tumor-derived HLA class I
molecules may contribute to induce such
alterations.
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