To assess whether aberrant IFN-γ production by CD4+ T cells in WSX-1−/− mice during infection [3]–[7] was simply due to WSX-1-mediated repression of T-bet expression within the effector population, or was also due to the suppression of T-bet+Th1 cell functionality on a cell per cell basis, we examined the capacity of splenic T-bet+ effector CD4+ T cells from WT and WSX-1−/− mice to produce IFN-γ and TNF following in vitro Phorbol 12-Myrisate 13-Acetate (PMA)/ionomycin restimulation. Here, IFNG is linked to infection.