Hence, our data establishes two significant attributes of inflammasome activation during parasite infection: 1) in the absence of TLR11 recognition, the inflammasome and IL-18 is critical for robust TH1 effector function; and 2) they provide pivotal evidence as to why IL-12 alone is insufficient to rescue Myd88-/- mice during T. gondii infection. This evidence concerns the gene MYD88 and parasitic infectious disease.