IFNA1 and infection: In follow-up analyses, Osokine and colleagues revealed that this switch occurred in an IFN-I-dependent manner wherein the absence of IFN signaling, TH1 responses were maintained; in the presence of IFN-I, the cytokine actively suppressed the emergence of de novo TH1 cells in a pre-programed function that occurred early in the priming stages of the infection (49).