DNA damage and type I interferons (IFNs) contribute to inflammatory responses after traumatic brain injury (TBI). TBI-induced activation of microglia and peripherally-derived inflammatory macrophages may lead to tissue damage and neurological deficits. Here, we investigated the role of IFN-β in secondary injury after TBI using a controlled cortical impact model in adult male IFN-β-deficient (IFN-β) mice and assessed post-traumatic neuroinflammatory responses, neuropathology, and long-term functional recovery.
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