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Immunobiology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
The importance of TNF-
in host defense to the intracellular
parasite, Toxoplasma gondii, was investigated in mice
lacking both the p55 and p75 receptors for this cytokine. Upon i.p.
infection with the avirulent ME49 strain, knockout mice were capable of
limiting acute i.p. infection, but succumbed within 3 to 4 wk to a
fulminant necrotizing encephalitis. Receptor-deficient mice harbored
higher cyst burdens and exhibited uncontrolled tachyzoite replication
in the brain. The lack of TNF receptors did not adversely affect the
development of a type 1 IFN-
response. In vitro studies with
peritoneal macrophages stimulated with IFN- and tachyzoites
indicated that under limiting concentrations of IFN-, nitric
oxide-mediated toxoplasmastatic activity is TNF- dependent. However,
this requirement is overcome by increasing the dose of IFN-.
Furthermore, both ex vivo and in vivo studies demonstrated that
inducible nitric oxide synthase induction in the peritoneal cavity and
brain is unimpaired in receptor-deficient mice. Thus, TNF-dependent
immune control of T. gondii expansion in the brain involves
an effector function distinct from inducible nitric oxide synthase
activation.
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