In vitro correction of antigen-induced immune suppression: effects of poly(A) poly(U) and prostaglandin E

Incubation of SJL or DBA/1 mouse spleen cells with poly(lTyr, lGlu)-polylPro—polylLys, (T, G)-Pro—L in vitro reduced the immune response potential of the cells to this immunogen as tested by adoptive transfer into irradiated, syngeneic recipients, followed by immunization with (T, G)-Pro—L in complete Freund's adjuvant. This reduction in immunocompetence was antigen-specific, since incubation with another antigen (rabbit immunoglobulin G) did not result in a suppression of responsiveness of the cells to subsequent in vivo immunization with (T, G)-Pro—L. Incubation of the spleen cell-(T, G)-Pro—L mixture in the presence of either prostaglandin E₁(PGE₁) or polyadenylic-polyuridylic acid (poly(A)·poly (U)) restored the immune response potential to the normal level. Incubation of (T, G)-Pro—L with spleen cells had no effect on cyclic AMP accumulation, whereas incubation of PGE₁ with the cells stimulated cyclic AMP production, irrespective of the presence of antigens. In contrast, the level of cyclic AMP was not affected by poly(A) · poly(U). The difference in cyclic AMP accumulation suggests that PGE₁ and poly(A) · poly(A) modify immune responsiveness by different mechanisms. The above observations were verified both in SJL and DBA/1 mice, which are the respective genetic high and low responders to (T, G) -Pro—L. This implies that the modifications of responsiveness described are not related to the genetic control of immune response to this immunogen.