Immunity to the opportunistic pathogen, Toxoplasma gondii, is highly depend
ent upon the effector activity of IFN-gamma-producing T lymphocytes. While
IFN-gamma is required to survive infection, an understanding of its functio
n remains incomplete. During infection, T. gondii simultaneously induces do
wnregulatory antiinflammatory cytokines, thereby avoiding major host pathol
ogy mediated by proinflammatory cytokines such as IFN-gamma. The ability to
induce the correct balance between these two opposing host responses likel
y accounts for the success of this organism as a parasite. (C) Elsevier, Pa
ris.