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How TGF\u03b2 signaling to microglia influences pathological retinal neuroinflammation is unclear. We discovered that ablation of the TGF\u03b2 receptor, TGFBR2, in retinal microglia of adult mice induced abnormal microglial numbers, distribution, morphology, and activation status, and promoted a pathological microglial gene expression profile. TGFBR2-deficient retinal microglia induced secondary gliotic changes in M\u00fcller cells, neuronal apoptosis, and decreased light-evoked retinal function reflecting abnormal synaptic transmission. While retinal vasculature was unaffected, TGFBR2-deficient microglia demonstrated exaggerated responses to laser-induced injury that was associated with increased choroidal neovascularization, a hallmark of advanced exudative AMD. These findings demonstrate that deficiencies in TGF\u03b2-mediated microglial regulation can drive neuroinflammatory contributions to AMD-related neurodegeneration and neovascularization, highlighting TGF\u03b2 signaling as a potential therapeutic target.<\/jats:p>","DOI":"10.7554\/elife.42049","type":"journal-article","created":{"date-parts":[[2019,1,8]],"date-time":"2019-01-08T08:40:32Z","timestamp":1546936832000},"source":"Crossref","is-referenced-by-count":83,"title":["Absence of TGF\u03b2 signaling in retinal microglia induces retinal degeneration and exacerbates choroidal neovascularization"],"prefix":"10.7554","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8396-6625","authenticated-orcid":true,"given":"Wenxin","family":"Ma","sequence":"first","affiliation":[{"name":"Unit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, United 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