Myd88-deficient animals are highly susceptible to infection by multiple pathogens, including T. cruzi, and exhibit diminished Th1 differentiation, which has been attributed to defective IL-12 production by APCs, as a consequence of poor TLR signaling (Campos et al., 2004; Fremond et al., 2004; Scanga et al., 2002; Seki et al., 2002; Muraille et al., 2003). This evidence concerns the gene MYD88 and infection.