Hypoxic-ischemic encephalopathy is a major cause of neonatal death and long-term disability globally. Subsequent inflammation after the brain injury has been identified as an important factor for neurological outcomes. Most studies have focused on early immunological changes following cerebral ischemia, but this strategy excludes many children from therapy since they present too late. Our group was the first to find long-lasting inflammation with activated T cells in the brain parenchyma up to five months after cerebral hypoxia-ischemia in rodents, and to show that peripheral lymphocytes in animals exposed to neonatal brain injury proliferate in response to brain antigens several months later. However, the characterisation of lymphocyte clusters, the distribution of lymphocytes to specific brain regions, and their communication with other cells remain unexplored. In this study, we aim to characterize the temporal, regional, and transcriptional pattern of T cell activation in the brain, meninges, spleen, and blood after hypoxic-ischemic injury in neonatal mice using spatial transcriptomics, single-cell RNAseq, and FACS. Our ultimate goal is to identify novel treatments to reduce the injury size and improve neurological outcomes by modulating the immune response.