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However, the precise role and mechanism of PD\u2010L1 in AKI remains largely elusive. In this study, we found that PD\u2010L1 was primarily expressed in proximal tubules and significantly upregulated in both murine models of AKI and renal biopsy samples from AKI patients. Genetic specific deletion of PD\u2010L1 in mouse tubular epithelial cells (TECs) exacerbated renal injury in ischemia\u2010reperfusion injury\u2010induced AKI. Mechanistically, PD\u2010L1 was found to interact with BRCA1 and increase BRCA1 expression to safeguard TECs against DNA damage, thereby promoting cellular proliferation and suppressing apoptosis. To translate these findings into a potential therapeutic strategy, we developed a CGA\u2010functionalized extracellular vesicle delivery system for targeted delivery of PD\u2010L1 to injured TECs. This system efficiently restored PD\u2010L1 expression and alleviated DNA damage of TECs in both TEC\u2010specific PD\u2010L1 knockdown and T\u2010cell knockout AKI mouse models. Collectively, these findings uncover a novel function of PD\u2010L1 in promoting adaptive TEC repair through BRCA1 interaction, independent of its canonical immunomodulatory function of T cells, and suggest that PD\u2010L1 supplementation may represent a promising therapeutic strategy for AKI.<\/jats:p>","DOI":"10.1002\/advs.75428","type":"journal-article","created":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T15:36:04Z","timestamp":1777304164000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["T Cell\u2010Independent Role of PD\u2010L1 in Kidney Repair: Mitigation of Tubular DNA Damage via PD\u2010L1\/BRCA1 Interaction Following AKI"],"prefix":"10.1002","volume":"13","author":[{"given":"Wei","family":"Jiang","sequence":"first","affiliation":[{"name":"Institute of Nephrology Zhongda Hospital School of Medicine Southeast University  Nanjing Jiangsu China"},{"name":"Department of Geriatric Geriatric Hospital 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