Abstract
Prostaglandin (PG) E2 inhibited CD 4+ cell proliferation stimulated with immobilized anti-CD 3 monoclonal antibody (mAb), 64.1 in a dose-dependent fashion. This inhibition was due to the suppression of interleukin 2 (IL 2) production, but not to that of IL 2 receptor expression. PGE2 decreased IL 2 mRNA level at a pretranslational level in CD 4+ cells. Phorbol myristate acetate (PMA) or mAb 9.3, when present in the culture, reversed PGE2-mediated inhibition of CD 4+ cell proliferation almost to the control level. IL 2 production by CD 4+ cell was highly increased in the presence of PMA or mAb 9.3 with immobilized mAb 64.1. This increase was also strongly inhibited by PGE2 in a dose-dependent manner. The level of IL 2 production by PMA or mAb 9.3 even in the presence of the highest concentration of PGE2 was higher than that of IL 2 produced by non-stimulated CD 4+ cells.
It is, therefore, suggested that the reverse effect of PMA or mAb 9.3 on the PGE2-mediated inhibition of CD 4+ cell proliferation may be due to the excess production of IL 2 by the PMA-or mAb 9.3-stimulated cells.
