TCR-ALPHA-BETA(-LYMPHOCYTES EXPRESS NKR-P1 WHILE THE ANTITUMOR-ACTIVITY OF TCR-GAMMA-DELTA(+) T-LYMPHOCYTES IS NOT CORRELATED TO NKR-P1 EXPRESSION() ANTITUMOR CYTOLYTIC T)

The CD8 alpha alpha homodimer as well as the NK cell receptor-protein 1 (NKR-P1) have been implicated to be preferentially expressed by T ce lls that develop extrathymically. We have earlier shown that intraperi toneal administration of radiated syngenetic W439 lymphoma cells in ra t induces tumor-specific cytotoxic T cells (CTL) expressing the TCR al pha beta receptor as well as the TCR gamma delta receptor. In the pres ent study we have addressed the expression of CD8 alpha alpha/alpha be ta and NRR-P1 on these CTL and their correlation to cytotoxicity activ ity against the W439 tumor. The induced CD8(+) T cells differentiated to effective cytotoxic cells regardless of the CD8 composition, NKR-P1 (+) T cells expressing CD8 were found in the peritoneal cavity of untr eated rats and this cell population was markedly increased upon lympho ma immunization. Both TCR alpha beta(+) cells and TCR gamma delta(+) c ells expressing NKR-P1 showed high cytotoxicity against the tumor. TCR gamma delta(+) NKR-P1(-) cells were also cytotoxic against the tumor, while TCR alpha beta(+) NKR-P1(-) cells showed no cytotoxicity. NKR-P 1(+) T cells (TCR alpha beta(+) and TCR gamma delta(+)) were not cytot oxic against NK sensitive targets, which contradicts earlier data impl icating a correlation between the expression of NKR-P1 and MHC-unrestr icted cytotoxicity. In conclusion, TCR alpha beta(+) anti-lymphoma CTL express high levels of LFA-1 and NKR-P1, while the TCR gamma delta(+) CTL are not dependant on NKR-P1. These results suggest that NKR-P1 ha s a different function within the TCR alpha beta(+) CTL than within th e TCR delta gamma(+) CTL in the recognition process of these lymphoma cells. (C) 1996 Academic Press, Inc.