Abstract
Parasitic infections are important causes of disease in the developing world and, since the advent of AIDS, the developed world. Over the past decade, in vitro and in vivo studies have established the important role that biological response modifiers play in pathogenesis of parasitic disease. These basic studies have resulted in successful clinical trials of interferon gamma (IFN-γ) in human leishmaniasis. Toxoplasmic encephalitis is a major opportunistic infection in patients with AIDS. and current therapy is often problematic. IFN-γ has been shown in in vitro and in vivo animal studies to be critical for host defence against Toxoplasma gondii. Tumour necrosis factor alpha plays a critical role in mediating IFN-γ effect in vitro, but its role in vivo is under further study. lnterleukin (1L)-6 and IL-10 have both recently been shown to enhance T gondii replication in vitro and to antagonize the beneficial effects of IPN-γ. In addition, in certain mouse strains. IL-6 has been shown to worsen mortality from T gondii infection. Future strategies for therapy of T gondii may include administration of exogenous IFN-γ or IL-12 with or without antibody to antagonistic cytokines such as IL-6 (or possibly IL-10).