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Using fate mapping, the authors demonstrate that kidneys from adult mice contain four subsets of DCs unique age-dependent differences in DCs and macrophages. Renal embryonic-derived macrophages are replaced shortly after birth by phenotypically similar cells arising from hematopoiesis. In adults, these are generated from DC progenitors. In two models of renal injury, cells resembling embryonic-derived macrophages reappear in inflamed kidneys as a result from MHCII downregulation from renal dendritic cells. Understanding age-dependent developmental aspects in these cells of immune-modulatory and antigen-presenting function may help scientists develop therapies targeting them.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Mononuclear phagocytes (MPs), including macrophages, monocytes, and dendritic cells (DCs), are phagocytic cells with important roles in immunity. The developmental origin of kidney DCs has been highly debated because of the large phenotypic overlap between macrophages and DCs in this tissue.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used fate mapping, RNA sequencing, flow cytometry, confocal microscopy, and histo-cytometry to assess the origin and phenotypic and functional properties of renal DCs in healthy kidney and of DCs after cisplatin and ischemia reperfusion\u2013induced kidney injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Adult kidney contains at least four subsets of MPs with prominent\n                      <jats:italic toggle=\"yes\">Clec9a<\/jats:italic>\n                      -expression history indicating a DC origin. We demonstrate that these populations are phenotypically, functionally, and transcriptionally distinct from each other. We also show these kidney MPs exhibit unique age-dependent developmental heterogeneity. Kidneys from newborn mice contain a prominent population of embryonic-derived MHCII\n                      <jats:sup>neg<\/jats:sup>\n                      F4\/80\n                      <jats:sup>hi<\/jats:sup>\n                      CD11b\n                      <jats:sup>low<\/jats:sup>\n                      macrophages that express T cell Ig and mucin domain containing 4 (TIM-4) and MER receptor tyrosine kinase (MERTK). These macrophages are replaced within a few weeks after birth by phenotypically similar cells that express MHCII but lack TIM-4 and MERTK. MHCII\n                      <jats:sup>+<\/jats:sup>\n                      F4\/80\n                      <jats:sup>hi<\/jats:sup>\n                      cells exhibit prominent\n                      <jats:italic toggle=\"yes\">Clec9a-<\/jats:italic>\n                      expression history in adulthood but not early life, indicating additional age-dependent developmental heterogeneity. In AKI, MHCII\n                      <jats:sup>neg<\/jats:sup>\n                      F4\/80\n                      <jats:sup>hi<\/jats:sup>\n                      cells reappear in adult kidneys as a result of MHCII downregulation by resident MHCII\n                      <jats:sup>+<\/jats:sup>\n                      F4\/80\n                      <jats:sup>hi<\/jats:sup>\n                      cells, possibly in response to prostaglandin E2 (PGE2). RNA sequencing further suggests MHCII\n                      <jats:sup>+<\/jats:sup>\n                      F4\/80\n                      <jats:sup>hi<\/jats:sup>\n                      cells help coordinate the recruitment of inflammatory cells during renal injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Distinct developmental programs contribute to renal DC and macrophage populations throughout life, which could have important implications for therapies targeting these cells.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019040419","type":"journal-article","created":{"date-parts":[[2020,1,13]],"date-time":"2020-01-13T17:05:45Z","timestamp":1578935145000},"page":"257-278","source":"Crossref","is-referenced-by-count":90,"title":["The Kidney Contains Ontogenetically Distinct Dendritic Cell and Macrophage Subtypes throughout Development That Differ in Their Inflammatory Properties"],"prefix":"10.1681","volume":"31","author":[{"given":"Natallia","family":"Salei","sequence":"first","affiliation":[{"name":"Walter Brendel Centre of Experimental Medicine, University Hospital Munich,"},{"name":"Institute for Cardiovascular Physiology and Pathophysiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan","family":"Rambichler","sequence":"additional","affiliation":[{"name":"Walter Brendel Centre of Experimental Medicine, University Hospital Munich,"},{"name":"Institute for Cardiovascular Physiology and Pathophysiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johanna","family":"Salvermoser","sequence":"additional","affiliation":[{"name":"Walter Brendel Centre of Experimental Medicine, University Hospital Munich,"},{"name":"Institute for Cardiovascular Physiology and Pathophysiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nikos 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