Cell-mediated immune responses to syngeneic ultraviolet-induced tumours. V. Assessment of accessory and antigen-presenting cell capabilities of normal and ultraviolet-irradiated mice in the generation of anti-tumour cytotoxic effector cells in vitro.

Draining lymph nodes (DLN) from tumour immunized mice were found to contain a population of radiation resistant, Thy 1-, Ia+ antigen-presenting cells (APC) which can stimulate normal lymphocytes to differentiate into anti-tumour CTL in vitro. APC from both normal and ultraviolet (u.v.)-irradiated tumour immunized animals were compared and exhibited equivalent functional capabilities. DLN from tumour immunized u.v.-irradiated animals were also found to contain primed T cells which could differentiate into functional anti-tumour cytotoxic T lymphocytes (CTL) with the same kinetic profile as DLN cells from normal tumour immunized mice. These results indicate that u.v. irradiation does not cause a generalized depression in either the capability of APC in u.v.-irradiated mice to process and present tumour antigens, or in the ability of u.v.-exposed animals to be primed to tumour antigens. A decrease in splenic accessory cell function was detected in animals which had received 1 week of daily 30 min u.v. exposures. The decrease in splenic accessory cell function appears to be transient, however, as no decrease in this capability was found in splenic cells obtained from animals which had received daily u.v. exposures for longer periods of time (5 weeks to 5 months). Finally, the spleens of u.v.-irradiated, tumour-bearing mice were found to contain a population of cells which could impart partial protection against tumour growth in vivo. The results of the experiments presented here indicate that normal and u.v.-irradiated animals are capable of responding similarly in the afferent phases of immune responses to syngeneic tumour antigens, and suggest that u.v.-induced T-suppressor cells mediate their immunoregulatory effects at a stage late in the generation of effective anti-tumour immune responses.