Gamma-interferon is the factor in lymphokine that activates human macrophages to inhibit intracellular Chlamydia psittaci replication.

We have demonstrated previously that mitogen-induced lymphokines activate human monocyte-derived macrophages to inhibit the intracellular replication of Chlamydia psittaci. To identify the factor(s) in crude lymphokines responsible for this antimicrobial effect, we tested human Con A-induced lymphokines for interferon activity. We also attempted to neutralize the lymphokines with a monoclonal antibody directed against human gamma-interferon and examined the ability of partially purified human gamma-interferon to induce macrophage antichlamydial activity. The lymphokine-induced antichlamydial effect was measured by the inhibition of chlamydial inclusion formation in Giemsa-stained macrophage cultures. Our lymphokines were found to be rich in gamma-interferon; treatment of cells for 48 hr before infection with lymphokines containing 300 U/ml of interferon resulted in an 89% inhibition of chlamydial growth. This lymphokine effect was completely abolished by monoclonal antibody against human gamma-interferon, but not by antisera against human alpha- or beta-interferons. In addition, partially purified human gamma-interferon alone induced macrophages to restrict chlamydial growth by 95%. We conclude that it is the gamma-interferon present in human Con A-induced lymphokines that activates monocyte-derived macrophages to inhibit chlamydial replication.