The role of recombinant murine beta interferon (rMuIFN-β) and recombinant human IFN-β (rHuIFN-β) in resistance to Toxoplasma gondii was examined. rMuIFN-β protected mice against a lethal infection with the parasite. The protective effect appeared to depend on the concomitant release of gamma interferon. rMuIFN-β did not activate murine peritoneal macrophages to inhibit or kill T. gondii whether used alone or in combination with lipopolysaccharide (LPS). rHuIFN-β did not activate human monocyte-derived macrophages to inhibit or kill T. gondii when 5-day-old monocyte-derived macrophages were used. In contrast, significant killing of T. gondii was noted when 10-day-old monocyte-derived macrophages were used. The addition of LPS enhanced this effect. These results revealed a role for IFN-β in the mechanisms of defense against T. gondii and suggest its potential use in the treatment of toxoplasmosis in humans.
