The escalation of infection with this mutant strain was associated with the production of pro-inflammatory cytokines such as IL-12, IL-17, IFN-ɣ and reduced secretion of IL-10, IL-4, and TGF-β in the placenta.85 Treatment of T. gondii-infected dams with TGF-β decreased resorption rates, improved fetal weights and diminished inflammation.86,87 This improved pregnancy outcome was linked to a TGF-β-mediated reduction of dNK-cell cytotoxicity and IFN-ɣ production.86 Here, TGFB1 is linked to infection.