Figure 13. Hypothetical model for the role of ETE in host defense.

Monocytes emigrating from blood vessels at a site of T. gondii infection encounter both activating signals, such as IFNγ, and parasites. The resulting macrophage is non-permissive if activation occurs first, since infection is followed by nitric oxide (NO) production, whereas it becomes relatively permissive (a ‘haven’) if infection occurs first, due to parasite-mediated suppression of IFNγ signaling. ETE forces parasite recycling from disrupted havens, resulting in a net transfer to non-permissive host cells that favors host defense.