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. Author manuscript; available in PMC: 2010 Nov 1.
Published in final edited form as: Trends Parasitol. 2009 Sep 9;25(11):491–494. doi: 10.1016/j.pt.2009.07.009

Figure 1.

Figure 1

Representation of the interactions between T. gondii molecules and host innate immunity signaling. (A) Free GPI of T. gondii binds with TLR2 or TLR4, resulting in transcription TNF-α through NF-kB. (B) T. gondii profilin induces IL-12 via TLR11/MyD88. (C) T. gondii cyclophilin interacts with CCR5 that signals through a Gi-like protein to increase IL-12 transcription. (D) ROP16 is released into the host cell upon T. gondii penetration causing activation of STAT3/6 which results in a decrease of IL-12. (E) T. gondii has lipoxygenase activity. A decrease in IL-12 is seen in response to the downregulation of CCR5 by lipoxin A4 generated by soybean lipoxygenase.