IFNG and infection: We next investigated the relative contribution of TLR11 and Casp1/11 in the regulation of TH1 immunity to T. gondii. Infection of TLR11-/- mice unexpectedly revealed TLR11-deficiency played no obvious role in the initiation of a CD4+ TH1 response towards T. gondii. This was in sharp contrast to TLR11xCasp1/11-deficient mice that demonstrated a profound reduction in both frequency and absolute numbers of CD4+IFN-γ+ T cells at the site of infection (Fig 4A–4C).