During the acute phase of the infection, a Th1 response characterized by increased levels of IFN-γ, tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1) and IL-6 is elicited, later modulated towards the Th2 side of reactions, i.e., production of immunoglobulin E and eosinophilia driven by IL-4 and IL-5 [22,23]. Here, IFNG is linked to infection.