In addition, we show that both MIC1 and MIC4 on the parasite surface contribute to the secretion of IL-12 by macrophages and DCs during in vitro infection, but only MIC1 plays a significant role during in vivo infection, demonstrated by its ability to promote a dysregulated induction of systemic levels of IFN-γ and a proinflammatory cytokine storm that leads to acute mortality during murine infection. Here, IFNG is linked to infection.