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Microglia are transcriptionally heterogenous, suggesting that distinct microglial states confer discrete roles. Currently, little is known about how dynamic these states are, the cues that promote them, or how they impact microglial function. In the developing retina, we previously found a significant proportion of microglia express CD11c (Integrin \u03b1X,\n                    <jats:italic>Itgax,<\/jats:italic>\n                    subunit of complement receptor 4) which has also been reported in other developmental and disease contexts. Here, we sought to understand the regulation and function of CD11c+ microglia. We found that CD11c+ microglia track with prominent waves of neuronal apoptosis in postnatal retina. Using genetic fate mapping, we provide evidence that microglia transition out of the CD11c state to return to homeostasis. We show that CD11c+ microglia have elevated lysosomal content and contribute to the clearance of apoptotic neurons, and found that acquisition of CD11c expression is partially dependent upon the TAM receptor AXL. Using selective ablation, we found CD11c+ microglia are not uniquely critical for phagocytic clearance of apoptotic cells. Together, our data suggest that CD11c+ microglia are a transient state induced by developmental apoptosis rather than a specialized subset mediating phagocytic elimination.\n                  <\/jats:p>","DOI":"10.1002\/glia.24674","type":"journal-article","created":{"date-parts":[[2025,1,20]],"date-time":"2025-01-20T00:33:11Z","timestamp":1737333191000},"page":"1077-1089","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["<scp>CD11c<\/scp>\n                    \u2010Expressing Microglia Are Transient, Driven by\u00a0Interactions With Apoptotic Cells"],"prefix":"10.1002","volume":"73","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1890-8036","authenticated-orcid":false,"given":"Nathaniel","family":"Ghena","sequence":"first","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"},{"name":"Interdepartmental Program in Neuroscience University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah R.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacqueline M.","family":"Roberts","sequence":"additional","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmalyn","family":"Irvin","sequence":"additional","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4907-6028","authenticated-orcid":false,"given":"Joon","family":"Schwakopf","sequence":"additional","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alejandra","family":"Bosco","sequence":"additional","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica L.","family":"Vetter","sequence":"additional","affiliation":[{"name":"Department of Neurobiology University of Utah School of Medicine  Salt Lake City Utah USA"},{"name":"Interdepartmental Program in Neuroscience University of Utah  Salt Lake City Utah 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