Abstract
Lymphokine-activated killer (LAK) cells can be generated by the incubation of peripheral blood mononuclear cells (PBMC) in the presense of interleukin 2 (IL 2). However, activity of these cells are frequently deppressed in tumor bearing hosts. In order to analyze a mechanism inhibiting induction of LAK activity, the effect of adherent cells on induction of LAK activity was investigated in the patients with hepatocellular carcinoma (HCC) and liver cirrhosis (LC).
Though LAK activity from nonadherent PBMC of the patients with HCC was deppressed in the presense of low concentration of IL2, sufficient activity was induced by high-dose of IL 2.
Adherent cells of the patients with HCC inhibited induction of LAK activity and this suppression was prevented by adding indomethacin. High concentration of PGE2 was detected in the culture medium of LAK induction system in the presense of adherent cells of the patients with HCC. The same concentration of PGE2 added in LAK induction system of normal controls suppressed LAK induction from NK cells in the early phase.
These results suggest that PGE2 produced by adherent cells inhibits LAK induction from NK cells in early phase in the patients with HCC.
