At 48 h post-infection, there is increased production of type I IFNs (IFN-α and IFN-β) and an increase in IFN-γ released by NK cells, which promotes APC maturation, positive regulation of co-stimulatory molecules, processing, and antigen presentation toward Th1 polarization [17], while simultaneously suppressing innate lymphoid cell-mediated immunopathology (ILC2) [18]. Here, IFNB1 is linked to infection.