IFNB1 and infection: Additional increase in IFN-β or IFN-I signaling, for example, in the case of traumatic infection or an aged brain, exacerbates disease outcomes in patients and mice, whilst loss of Ifnb and anti-IFNAR1 treatment in mice attenuates the damage from TBI (133, 134, 196–198), further demonstrating the neurotoxic capacity of IFN-Is.