Clonally expanded targetable natural killer-like T cells seed the aged spinal cord to disrupt wound healing [scRNA-seq]

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. Here, we hypothesized 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 by conducting single-cell RNAseq (scRNAseq) experiments from the spinal cord of young and aged mice preceding and following a SCI. Young and aged mouse spinal cord segments were collected from conditions including naive, 14 days, and 28 days after spinal cord injury. After, cells were isolated for single cell RNAseq. Three biological replicates were included in each condition.