Immunostimulation by XXXX .

@entity137 @entity4878 @entity2047 @entity5 @entity19 @entity3512 @entity1778 @entity1968
@entity4878 have been shown to inhibit @entity5 growth in several model systems. In this paper evidence that immune effectors are important for this effect is discussed. Injection of @entity1968 (RA) into @entity19 before challenge with allogeneic or syngeneic @entity5 cells results in a strong increase in cell-mediated @entity137 specific for the respective @entity5 . This stimulation appears to be due to effects taking place before or during the induction phase rather than the effector phase of cell-mediated cytolysis. The effector cells responsible for @entity137 express the @entity3512 , are H-2 specific and are therefore T killer cells. The induction of T cell-mediated @entity137 requires the participation of the lymphokine interleukin 2 ( @entity2047 ). The possibility was tested that RA directly or indirectly influences the production of @entity2047 and thereby stimulates the induction of T killer cells. Results indeed show that RA-injected @entity19 display an increased capacity to produce @entity2047 upon stimulation of their splenocytes in a mixed lymphocyte reaction. It appears therefore that RA has an effect on T cells that are destined to produce @entity2047 upon antigenic challenge. Since @entity2047 plays a role not only in the induction of specific cytotoxic T cells but also in the induction of natural killer (NK) cells, RA was also tested in a model system in which NK cells appear to play an important protective role. Results showed that split-dose irradiated @entity19 that lose their NK activity and subsequently develop @entity1778 can be protected from leukaemogenesis either by reconstitution with NK cells or by injection with RA. The question of whether this effect is due to stimulation of immune effectors or is a direct effect on the preleukaemic cells is discussed.
