INHIBITION OF MACROPHAGE-INDUCED, ANTIGEN-SPECIFIC T-CELL PROLIFERATION BY POLY I-C ROLE OF SUPPRESSOR MACROPHAGES

Poly I:C treatment can inhibit the ability of macrophages (M phi) to i nduce antigen-specific T-cell proliferation. This study investigated w hether this inhibition is the result of suppresssor or cytotoxic activ ity. Pretreatment of M phi with indomethacin in vivo, in vitro or both failed to reverse the inhibition of T-cell proliferation induced by p oly I:C-treated, keyhole limpet haemocyanin (KLH)-pulsed M phi, sugges ting that prostaglandin production does not mediate the inhibition of T-cell profileration. The transfer of supernatants from cultures conta ining poly I:C-treated, KLH-pulsed M phi to cultures containing saline -treated, KLH-pulsed M phi and T cells did not inhibit T-cell prolifer ation, suggesting that the inhibition of T-cell proliferation by poly I:C is not mediated by the production of soluble suppressor factors. A s addition of poly I:C-treated, KLH-pulsed M phi to cultures containin g saline-treated, KLH-pulsed M phi did not significantly inhibit KLH-s pecific T-cell proliferation, the inhibition of T-cell proliferation i s also not mediated by direct cell contact or short-range soluble supp ressor factors. In addition, poly I:C-treated, KLH-pulsed M phi did no t induce cytolysis of syngeneic T cells. These results indicate that c ytotoxic or suppressor effector functions of M phi are not involved in the mechanism by which poly I:C inibits M phi-induced, antigen-specif ic T-cell proliferation.