Host persistence: exploitation of anti-inflammatory pathways by Toxoplasma gondii.
Hosts that are infected with Toxoplasma gondii must mount a powerful immune response to contain dissemination of the parasite and to prevent mortality. After parasite proliferation has been contained by interferon-gamma-dependent responses, the onset of the chronic phase of infection is characterized by continuous cell-mediated immunity. Such potent responses are kept under tight control by a class of anti-inflammatory eicosanoid, the lipoxins. Here, we review such immune-containment strategies from the perspective of the host, which attempts to keep pro-inflammatory responses under control during chronic disease, as well as from the perspective of the pathogen, which hijacks the lipoxygenase machinery of the host for its own advantage, probably as an immune-escape mechanism.
Aliberti
Julio
J
Department of Immunology, Duke University Medical Center, Durham, North Carolina 27705, USA. julio.aliberti@duke.edu
D000818:Animals; D006790:Host-Parasite Interactions / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D044045:Lipoxins / Q000276:immunology*; D014122:Toxoplasma / Q000276:immunology* / Q000472:pathogenicity; D014123:Toxoplasmosis / Q000276:immunology* / Q000635:transmission
D044045:Lipoxins