Nonimmune Cells Contribute to Crosstalk between Immune Cells and Inflammatory Mediators in the Innate Response to Trypanosoma cruzi Infection
Figure 2
TLR-independent innate immune responses. Infection triggers increased intracellular Ca2+ concentration through interaction of bradykinin with the bradykinin B2 receptor (B2-R) among other mechanisms. Target innate immune cells utilize Ca2+ to activate the Ca-dependent signaling pathway leading to the activation of NFATc1. Intracellular T. cruzi is recognized by NOD1, activating NF-κB. T. cruzi is also recognized by unknown molecules leading to the activation of TBK1 and IRF3. Altogether the mechanisms participate in the induction of an effective immune response against the parasite.
