We have previously demonstrated that toll-like receptors (TLRs) are essential for host resistance against neosporosis, since MyD88 and TLR2 ablation produced pronounced effects over the development of a specific Th1 response, based on the classical IL-12/IFN-γ axis, during the course of infection (24, 53); other classes of receptors—as Nod2—are also relevant in the pathogenesis of the disease (30). This evidence concerns the gene MYD88 and infection.