Intestinal inflammation or parasitic infection favours the reprogramming of Foxp3⁺ T_REG cells into effector T cells and promotes host immunity.

<p>(<b>A–B</b>) TCRβ^−/− mice received GFPtg CD4⁺CD25⁺ T cells (0.3×10⁶). 14 days later Foxp3 expression within donor GFP⁺CD4⁺ T cells (<b>A</b>) and the frequency of total IFN-γ or IL-17 producing cells (<b>B</b>) in indicated tissues of recipient mice from one of 3 representative experiments (n>3) is shown. (<b>C–G</b>) TCRβ^−/− mice were infected or not (NI) with 5×10⁶ promastigotes of WT or GP63^−/− (KO) <i>L. major</i> into the right footpad 2 weeks prior reconstitution with GFPtgCD4⁺CD25⁺ T_REG cells (0.3×10⁶). (<b>C</b>) 4 weeks later, GFP⁺CD4⁺ T cells from draining (infected) and non-draining popliteal LN, perLN and mesLN were analyzed for Foxp3 expression. Footpad swelling (<b>D</b>), absolute number of infiltrated lymphocytes (<b>E</b>), and frequencies of IFN-γ producing CD4⁺ T cells (<b>F</b>) are shown in infected and non-infected sites. (<b>G</b>) The loss of Foxp3 expression by T_REG cells was compared between mice infected with WT or GP63^−/−<i>L. major</i> strains. Results are representative of 2 independent experiments with n = 4–5.