Some tumor cell lines and fresh tumor cells are killed by natural killer cell (NK cell), and NK cell is said to play an important role in antitumor immune defense mechanism.
This study was conducted in order to gain information about the cytotoxic activity of peripheral blood lymphocyte (PBL) and white blood cell (WBC) in patients with head and neck malignant tumor, and the change of that cytotoxic activity after therapy.
PBL and WBC were obtained from patients with malignant lymphoma and carcinoma in head and neck region before the beginning of therapy, and 2 weeks, 1 month, 3 months, and 6 months after the end of therapy. NK cell activity of these effector cells against K562 cells was tested by the method of 4-hour 51Cr-release assay. Autologous lymphocyte cytotoxicity (ALC) against biopsied lymphoma cells was also tested in patients with malignant lymphoma.
In the untreated patients, NK cell activity and ALC were reduced, and there was no significant difference between the cytotoxicity of PBL and that of WBC. It seemed that macrophages and granulocytes did not affect the cytotoxicity of PBL in vitro. Though no change of NK cell activity was noted in the posttreated period up to 6 months, increased ALC was observed, and furthermore the cytotoxicity of PBL against hot K562 cells was inhibited by cold autologous lymphoma cells in the cold target inhibition test. The incubation of PBL and WBC with OK432 for 20 hours in vitro resulted in the augmentation of NK cell activity and ALC. On the other hand, the incubation of those with mitomycin C (MMC) neither show the augmentation nor the reduction of the cytotoxic activity. No correlation was observed between the cytotoxic activity and the extent of the disease or immunological parameters (peripheral lymphocyte count, lmphocyte subset, lymphocyte blast formation test by PHA).
NK cell activity and ALC were reduced in the patients with malignant tumor, and the cytotoxic activity abainst autologous tumor cells was recovred in the posttreated patients. These results suggest that the recongtion of PBL to autologous tumor cells was augmented in the posttreated period.
