We find that small differences in the initial immune conditions (e.g. the state of T-helper cell polarization) and parasite dose can lead to vastly different infection outcomes depending on the strength of the feedback mechanisms.

This work is interesting because it provides a way to link standing immune phenotypes with disease susceptibility! We are now doing experiments to validate this model, and see what immune metrics we can use to predict parasite burdens and infection duration. So, stay tuned!