Neuropsychiatric complications including depression and cognitive impairment develop, persist, and worsen in the years after traumatic brain injury (TBI), negatively affecting life and lifespan. Inflammatory responses mediated by microglia are associated with the transition from acute to chronic neuroinflammation after TBI. Moreover, type I interferon (IFN-I) signaling is a key mediator of inflammation during this transition. Thus, the purpose of this study was to determine the degree to which a microglia-specific knockout of the stimulator of interferons (STING) influenced TBI-induced neuroinflammation, neuronal dysfunction, and cognitive impairment. Here, microglial inducible STING knockout (CX