Consistent with our in vitro findings, significant reductions in T-bet+ Treg cell frequencies were observed in both spleen and LP of CD11ccreIL27p28fl/fl mice with or without T. gondii infection (Fig. 7A and B), pointing to DCs as critical cellular sources of IL-27 responsible for promoting the development and function of Th1-Treg cells in both physiological and parasitic infection settings. The gene discussed is IL27; the disease is parasitic infectious disease.