The role of recombinant murine beta interferon (rMuIFN-beta) and recombinant human IFN-beta (rHuIFN-beta) in resistance to Toxoplasma gondii was examined. rMuIFN-beta protected mice against a lethal infection with the parasite. The protective effect appeared to depend on the concomitant release of gamma interferon. rMuIFN-beta did not activate murine peritoneal macrophages to inhibit or kill T. gondii whether used alone or in combination with lipopolysaccharide (LPS). rHuIFN-beta 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-beta in the mechanisms of defense against T. gondii and suggest its potential use in the treatment of toxoplasmosis in humans.
No takes yet. Share an insight, caveat, or question.
Orellana et al. (1991) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: