Clonally expanded targetable natural killer-like NKG7 T cells seed the aged spinal cord to disrupt myeloid-dependent wound healing

The wound healing ability of the central nervous system declines with aging. Spinal cord injury (SCI) has been increasingly affecting aged individuals, where functional impairment and mortality are highest. However, the aging-dependent mechanisms underpinning tissue damage and repair after SCI remain elusive, limiting effective interventions. We hypothesised that changes to the molecular and cellular signatures of the local spinal cord tissue microenvironment across the lifespan might affect spinal wound healing, axonal injury responses, and functional recovery. To test this hypothesis, we investigated the molecular and cellular signatures associated with the wound healing response after an experimental SCI in the mouse across the lifespan.To test this hypothesis, we initially conducted single-cell RNAseq (scRNAseq) experiments from the spinal cord of young and aged mice preceding and following a SCI.