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- W4223580167 abstract "Monocytes undergo phenotypic and functional changes in response to inflammatory cues, but the molecular signals that drive different monocyte states remain largely undefined. We show that monocytes acquire macrophage markers upon glomerulonephritis and may be derived from CCR2+CX3CR1+ double-positive monocytes, which are preferentially recruited, dwell within glomerular capillaries, and acquire proinflammatory characteristics in the nephritic kidney. Mechanistically, the transition to immature macrophages begins within the vasculature and relies on CCR2 in circulating cells and TNFR2 in parenchymal cells, findings that are recapitulated in vitro with monocytes cocultured with TNF-TNFR2-activated endothelial cells generating CCR2 ligands. Single-cell RNA sequencing of cocultures defines a CCR2-dependent monocyte differentiation path associated with the acquisition of immune effector functions and generation of CCR2 ligands. Immature macrophages are detected in the urine of lupus nephritis patients, and their frequency correlates with clinical disease. In conclusion, CCR2-dependent functional specialization of monocytes into macrophages begins within the TNF-TNFR2-activated vasculature and may establish a CCR2-based autocrine, feed-forward loop that amplifies renal inflammation." @default.
- W4223580167 created "2022-04-15" @default.
- W4223580167 creator A5003260180 @default.
- W4223580167 creator A5004554046 @default.
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- W4223580167 creator A5031554195 @default.
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- W4223580167 creator A5081489856 @default.
- W4223580167 creator A5086548867 @default.
- W4223580167 date "2022-04-11" @default.
- W4223580167 modified "2023-10-10" @default.
- W4223580167 title "Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2" @default.
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