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- W4313356468 abstract "Abstract Alternatively activated M2 macrophages accumulate during inflammation from the recruitment of inflammatory monocytes, or through the proliferation of tissue resident macrophages. Monocyte derived and tissue resident M2 macrophages are phenotypically and functionally distinct, with UCP1 expression being a unique feature of tissue resident cells. We now show that monocyte derived M2 macrophages can acquire some of the phenotypic features of tissue resident cells after long-term residence in tissues. In liver granulomas of S. mansoni infected mice, UCP1 expression and proliferating cells accumulate in the periphery of mature granulomas. Genetic fate mapping macrophages derived from CX3CR1(+) monocytes indicate that UCP1 expressing cells are derived from monocyte precursors. Conversion to a tissue resident phenotype is independent of Stat6, although Stat6 regulates macrophage proliferation both intrinsically and extrinsically. Vitamin A deficiency (VAD) leads to dysregulation of the balance between monocyte and tissue macrophage derived M2 cells. Liver granulomas of S. mansoni infected VAD no longer express UCP1 and GATA6, indicating a failure to adopt tissue resident phenotype, and are associated with increased mortality. Inflammatory macrophages transferred into VAD mice fail to convert to a tissue resident phenotype. Genetic fate mapping experiments in VAD mice confirmed the failure of inflammatory macrophages to adopt tissue resident macrophage features despite long term tissue residence. Retinoic acid treatment of VAD mice reverses some of the defects. Hence, retinoic acid may regulate the conversion of monocyte derived inflammatory M2 macrophages into a tissue resident phenotype." @default.
- W4313356468 created "2023-01-06" @default.
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- W4313356468 date "2016-05-01" @default.
- W4313356468 modified "2023-10-12" @default.
- W4313356468 title "Vitamin A deficiency disrupts conversion of inflammatory monocyte derived M2 macrophages into a tissue resident macrophage phenotype." @default.
- W4313356468 doi "https://doi.org/10.4049/jimmunol.196.supp.52.12" @default.
- W4313356468 hasPublicationYear "2016" @default.
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