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Conflicting effects on post-stroke functional recovery, however, are secondary to the differences in responding lymphocyte populations that shift immunophenotype with both ischemic injury and age. To better define CNS-localized B cell subsets, we used flow cytometry, single-cell RNA sequencing, and B cell receptor sequencing on B cells isolated from uninjured and post-stroke brains of aged male and female mice. We identified a novel B1b cell progenitor pool distinct from canonical pleural and peritoneal B1 niches. Trajectory analysis showed B1b progenitors transition into age-associated B cell (ABC) subsets, and clonal expansion of IgM+ ABCs (ABC\/B1b) and plasma cells following ischemic stroke. We also confirmed analogous ABCs and developing B cell populations in post-mortem human parenchymal tissue isolated from aged brain donors. These studies reveal unique B cell populations that proliferate within the aging CNS and are associated with impaired post-stroke functional recovery in mice. Identification of inflammatory, CNS-resident ABC\/B1b cells that are conserved across species is critical as they have the potential to be sequestered from peripheral immunotherapies and\/or contribute to age-related neurodegenerative diseases.<\/jats:p>","DOI":"10.64898\/2026.03.02.709112","type":"posted-content","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T19:10:19Z","timestamp":1772651419000},"source":"Crossref","is-referenced-by-count":0,"title":["Age-associated B cells (ABCs) develop from a CNS-localized progenitor pool into a pro-inflammatory phenotype after stroke"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-1528-6901","authenticated-orcid":false,"given":"Annabel M.","family":"McAtee","sequence":"first","affiliation":[{"name":"Department of Neuroscience, University of Kentucky, 741 S. 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