Taking into account that A2AR signaling can restore homeostasis by promoting Tregs generation and immunosupression (27) and inflammatory mediators such as IFN-γ can limit the Treg function and differentiation (65) and that IFN-γ was upregulated in the infectious foci of L. infantum (Figures 3A–F), we next evaluated whether the Th1-induced inflammation observed in the A2AR−/− mice could be related to compromised Treg functions during infection. The gene discussed is IFNG; the disease is infection.