Thus, early production of type I IFN, preceding the IFNγ response, might be crucial for the induction of an appropriate immune response (including: recruitment, differentiation, and survival of myeloid cells that control early infection, as well as the induction of dendritic cell maturation, and associated IL-12 production and T-lymphocyte priming), while a more chronic IFN type I response might increase disease susceptibility [50]. This evidence concerns the gene IFNG and infection.