We demonstrated that TLR4 signaling triggers an important early parasiticidal event against T. cruzi, which is dependent on the formation of NO and ROS and that splenocytes of Tlr4−/− infected mice display lower production of the proinflammatory cytokines IFN-γ and TNF-α, as well as of NO, when compared to WT B6 mice, what would explain the observed higher parasitemia levels in TLR4-deficient mice [31]. Here, TLR4 is linked to parasitic infectious disease.