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We report a mouse model allowing for selective depletion of a specific subset of kidney MPs that is based on a Cre-inducible lox-STOP-lox-diphtheria toxin receptor gene controlled by the endogenous CD64 promoter. Combined with specific targeting of conventional DC1 (cDC1) and cDC2, we revealed that CD64\n                    <jats:sup>+<\/jats:sup>\n                    MPs account for the reported ability of CD11c\n                    <jats:sup>+<\/jats:sup>\n                    cells to limit cisplatin nephrotoxicity, while cDC1 and cDC2 are dispensable. Our study highlights that individual MP subsets have unique functions in kidney pathology. Combined with various CRE drivers, CD64-lox-STOP-lox-diphtheria toxin receptor mice might be used to study CD64-expressing cells in other tissues.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2022311118","type":"journal-article","created":{"date-parts":[[2021,9,28]],"date-time":"2021-09-28T12:59:23Z","timestamp":1632833963000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":12,"title":["Selective depletion of a CD64-expressing phagocyte subset mediates protection against toxic kidney injury and failure"],"prefix":"10.1073","volume":"118","author":[{"given":"Natallia","family":"Salei","sequence":"first","affiliation":[{"name":"Walter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universit\u00e4t in Munich, 82152 Planegg-Martinsried, Germany;"},{"name":"Biomedical Center, Institute for Cardiovascular Physiology and Pathophysiology, Faculty of Medicine, Ludwig-Maximilians-Universit\u00e4t in 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