Resolution of Inflammation during Toxoplasma gondii Infection

Abstract

Upon Toxoplasma gondii host infection, a powerful immune response takes place in order to contain dissemination of the parasite and prevent mortality. Once parasite proliferation is contained by IFN-γ-dependent responses, nevertheless-, parasite immune escape prevents complete clearance characterizing the onset of the chronic phase of infection, with a continuous (and powerful) cell-mediated immunity. Such potent responses are kept under tight control by several, non-redundant mechanisms that control pro-inflammatory mediators. Including cytokines, such as members of the IL-10 family, TGF-beta, the membrane receptors, ICOS, CTLA4 and a class of anti-inflammatory eicosanoids, the lipoxins. In this chapter we address the host strategies that keep pro-inflammatory responses under control during chronic disease. On the other hand, we approach the perspective of the pathogen, which pirates the host's machinery to its own advantage as a part of the pathogen's immune-escape mechanisms.