Evidence suggests that the infection of retinal cells with T. gondii results in the expression of IL17 by resident cells (Müller cells, but maybe also Th17 T cells), which might be responsible for the recruitment into the retina of activated immune cells, facilitated by the increased permeability of the external blood-retinal barrier. These immune cells would be responsible for subsequent retinal lesions, probably also by suppression of Treg cells (not shown). At the same time, IL17 expression negatively interferes with IFNγ production, thereby diminishing the protective antiparasitic response. IFNγ, interferon gamma; IL17, interleukin 17; Treg, regulatory T cells.