N. Guerra et al., Killer inhibitory receptor (CD158b) modulates the lytic activity of tumor-specific T lymphocytes infiltrating renal cell carcinomas, BLOOD, 95(9), 2000, pp. 2883-2889
In this study, we showed that renal tumors contain substantial subsets of C
D8(+) p58(+) T cells, From 1 of these tumors, T cells were amplified in mix
ed lymphocytes-tumor cell cultures and p58(+) T cells were selected immunol
ogically, After expansion, phenotypic and functional features of p58(+) and
p58(-) T cells were examined. The p58(+) T cells expressed p58.2 receptor
and corresponded to CD3(+), CD8(+), T-cell receptor (TCR) alpha/beta(+) T c
ells that were CD56(+) and CD28(-). Functionally, p58(+) T cells showed a l
ow level of lytic activity against autologous tumor cells that was dramatic
ally and specifically increased by anti-p58.2 monoclonal antibody. On the o
ther hand, p58- CD8(+) T cells did not lyse autologous tumor cells and had
non major histocompatibility complex-restricted cytotoxicity against K562 a
nd Daudi cells. A p58(+) cytotoxic T lymphocyte (CTL) clone (4C7) with the
same characteristics as the p58(+) T-cell line was derived. This CTL clone
did not lyse autologous normal B cells but lysed several HLA-A1(+) renal tu
mor cell lines. Analysis of TCR repertoire diversity showed that the p58(+)
T-cell line contained 3 TCR rearrangements, whereas the TCR repertoire of
p58(-) T cells was polyclonal, Interestingly, TCR transcripts of p58(+) T c
ells and of CTL clone 4C7 were detected as prominent ex vivo in tumor cells
but not in peripheral blood mononuclear cells, suggesting that these cells
are antigen specific and amplified at the tumor site. (Blood, 2000;95:2883
-2889) (C) 2000 by The American Society of Hematology.