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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Trends Parasitol. 2011 Sep;27(9):388–393. doi: 10.1016/j.pt.2011.03.009

Figure 1. TLR activation in DC plays a central role in regulation of type I innate immunity.

Figure 1

Recent results demonstrated that the crucial function of TLR/MyD88 signaling in DCs in defense against T. gondii infection was to activate NK cells and inflammatory monocytes [18]. Although MyD88 function in DCs was not required for the recruitment of inflammatory cells into the peritoneum of T. gondii-infected mice, it was required for the vast majority of IL-12 production, which in turn was required for promoting IFN-γ production by NK cells and subsequent activation of the inflammatory monocytes and macrophages to allow them to kill the parasites [18]. This model demonstrates how innate cells cooperate in vivo to generate cell-mediated innate immunity to defend against a highly virulent intracellular pathogen.