The possibility of differential PVL induction in human and mouse tissues in human and mouse response is another potential confounding factor in extrapolating animal data to the human condition.
38, 39 With T. gondii, mouse responses are also based on toll-receptor MyD88, NF-κB, and MAP kinase signaling, resulting in defined inflammatory responses.
Measures on human skin using a thermistor showed a slight laser-induced increase in surface temperature (from 27.5°C to 30.5°C) over the 30 s stimulation period, indicating that KRT-ChR2 mouse responses were not due to laser heating of the skin.
T3 treatment increased biliary cholesterol secretion 3.1-fold in Abcg5+/+ mice, whereas in Abcg5−/− mice, this response was blunted.
Although CCK8s inhibited food intake in uninfected C57BL/6 mice, the response was virtually abolished in infected C57BL/6 mice.
We observed that BALB/c mice generated a robust dose-dependent increase in IL-4 production, while in C57BL/6 mice the response was lower (Fig. 3a, note log scales).
A similar mouse-specific response was observed at the level of individual genes.
In MPL-immunized mice this response was primarily seen upon stimulation with the CD8 T cell epitope.
In the SENCAR mice, positive response was seen with all four chemicals, however, FANFT gave an inconsistent response.
Strikingly, although p53 accumulated to high levels at mitochondria of treated wild-type mice, this response was absent in tissues lacking Pin1, suggesting that Pin1 is essential for mitochondrial localization and mitochondrial functions of p53 in vivo.
