ArticleThe Journal of experimental medicine2025
Prenatally derived macrophages support choroidal health and decline in age-related macular degeneration.
Article in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Tissue-resident macrophages maintain choroidal homeostasis by complement dependent and independent mechanisms.Journal of neuroinflammation · 2026Article
- Vitreoretinal Myeloid Cell Heterogeneity: Diverse Roles in Homeostasis, Immune Surveillance, and Pathophysiology.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Principles of resident tissue macrophages revealed by the eye.Advances in immunology · 2026Review
- TREM2 in age-related macular degeneration: a microglia-centered perspective in the retinal myeloid landscape.Frontiers in ophthalmology · 2026Review
- Targeting Diabetic Retinopathy with Human iPSC-Derived Vascular Reparative Cells in a Type 2 Diabetes Model.Cells · 2025Article
- Article
- The role of inflammation in myopic retinopathy.Frontiers in ophthalmology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Hallmark findings in age-related macular degeneration (AMD) include the accumulation of extracellular lipid and vasodegeneration of the choriocapillaris. Choroidal inflammation has long been associated with AMD, but little is known about the immune landscape of the human choroid. Using 3D multiplex immunofluorescence, single-cell RNA sequencing, and flow cytometry, we unravel the cellular composition and spatial organization of the human choroid and the immune cells within it. We identify two populations of choroidal macrophages with distinct FOLR2 expression that account for the majority of myeloid cells. FOLR2+ macrophages predominate in the nondiseased eye, express lipid-handling machinery, uptake lipoprotein particles, and contain high amounts of lipid. In AMD, FOLR2+ macrophages are decreased in number and exhibit dysfunctional lipoprotein metabolism. In mice, FOLR2+ macrophages are negative for the postnatal fate-reporter Ms4a3, and their depletion causes an accelerated AMD-like phenotype. Our results show that prenatally derived resident macrophages decline in AMD and are implicated in multiple hallmark functions known to be compromised in the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.