Abstract
Results: The treatment of BeWo cells with IL-10 and TGF-β1 favored T. gondii proliferation and these findings were associated with STAT-3 and Smad2 phosphorylation, respectively. Also, these cytokine treatments were able to downmodulate TNF-α and IL-6 production. A low concentration of IFN-γ was unable to control T. gondii infection, but was able to trigger STAT-1 phosphorylation and up-regulate IL-6 and IL-17A production, whereas a high concentration of IFN-γ was unable to activate STAT-1, but down-modulated IL-6 and TNF-α and increased T. gondii proliferation.
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