ArticleResearch square2026
Type I interferon signaling in microglia drives synaptic engulfment and neuronal loss following traumatic brain injury.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Type I interferon (IFN-I) signaling has emerged as a central regulator of neuroinflammation across diverse central nervous system disorders, including traumatic brain injury (TBI). While TBI is a leading cause of neurologic morbidity and mortality through young adulthood, there is a paucity of neuroprotective therapies available to clinicians. Recent work has demonstrated neuroprotection after global IFN-I deficiency, yet the cell-type-specific contributions to traumatic brain injury (TBI) and the mechanisms of immune modulation remain poorly defined. Using mice with microglia-specific IFN-I receptor deficiency, we show that loss of microglial IFN-I responsiveness suppresses microglial reactivity, reducing microglial accumulation, synaptic engulfment, antigen presentation, and T cell interactions after TBI. This attenuation preserves neuronal integrity and limits thalamic neuronal loss. Despite this neuroprotection, microglia-restricted IFN-I blockade reveals functional redundancy across CNS cell types, underscoring the multi-cellular nature of IFN-I signaling in the injured brain. Together, our findings delineate a microglial IFN-I-dependent pathway that exacerbates secondary injury after TBI and highlight both the therapeutic potential and inherent limitations of cell-type-targeted IFN-I modulation.
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