TCR alpha beta+ anti-tumor cytolytic T lymphocytes express NKR-P1 whilethe anti-tumor activity of TCR gamma delta+ T lymphocytes is not correlated to NKR-P1 expression.

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 cells that develop extrathymically. We have earlier shown that intraperitoneal administration of radiated syngeneic W439 lymphoma cells in rat induces tumor-specific cytotoxic T cells (CTL) expressing the TCR alpha beta receptor as well as the TCR gamma delta receptor. In the present study we have addressed the expression of CD8 alpha alpha /alpha beta and NKR-P1 on these CTL and their correlation to cytotoxicity activity 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 untreated rats and this cell population was markedly increased upon lymphoma immunization. Both TCR alpha beta+ cells and TCR gamma delta+ cells 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-P1+ T cells (TCR alpha beta+ and TCR gamma delta+) were not cytotoxic against NK sensitive targets, which contradicts earlier data implicating a correlation between the expression of NKR-P1 and MHC-unrestricted 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 has a different function within the TCR alpha beta+ CTL than within the TCR gamma delta+ CTL in the recognition process of these lymphoma cells.