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cells, csfr, intestinal, mice, pubmed, paneth, cell, expression, macrophages, article, crypts, stem, google, scholar, fig, analysis, blockade, cas, data, anticsfr, lgr, crypt, prolonged, mrna, gut, peyers, mab, epithelial, patches, micegroup, differentiation, bar, treatment, scale, fae, enteroids, central, nature, epithelium, csf, small, represent, macrophage, intestine, wnt, control, supplementary, factor, sections, homeostasis,

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nature portfolio privacy policy c57bl/6j wild-type mice advertising thermofisher scientific macrophage colony-stimulating factor macrophage colony-stimulating factor-1 paneth cell-derived α-defensins social media detection kits medical research council ns mann–whitney u-test medical research institute translational research institute reprints anti-csf1r-treated mice correlated mann–whitney u-test 10 µg/ml anti-csf1r mab inflammation research paneth cell α-defensins polyclonal anti-csf1r antibody cycling leucine-rich repeat rt–qpcr analysis shows anti-csf1r mab-treated mice intestinal stem-cell niche nature 459 nature 469 nature 462 nature 507 nature 525 nature 478 nature 530 nature 476 nature real-time quantitative pcr single-cell transcriptomics identify colony-stimulating factor colony-stimulating factor-1 colony-stimulating factor 1 open bars lgr5-expressing stem cells multiple-colour immunofluorescence histology rabbit anti-lysozyme mab graft-versus-host disease lysoszyme-expressing paneth cells nuclear factor-κb ligand middle panel csf1r-egfp reporter mouse lysozyme-expressing paneth cells differentiated cell types

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         description:Colony-stimulating factor 1 (CSF1) controls the growth and differentiation of macrophages.CSF1R signaling has been implicated in the maintenance of the intestinal stem cell niche and differentiation of Paneth cells, but evidence of expression of CSF1R within the crypt is equivocal. Here we show that CSF1R-dependent macrophages influence intestinal epithelial differentiation and homeostasis. In the intestinal lamina propria CSF1R mRNA expression is restricted to macrophages which are intimately associated with the crypt epithelium, and is undetectable in Paneth cells. Macrophage ablation following CSF1R blockade affects Paneth cell differentiation and leads to a reduction of Lgr5+ intestinal stem cells. The disturbances to the crypt caused by macrophage depletion adversely affect the subsequent differentiation of intestinal epithelial cell lineages. Goblet cell density is enhanced, whereas the development of M cells in Peyer’s patches is impeded. We suggest that modification of the phenotype or abundance of macrophages in the gut wall alters the development of the intestinal epithelium and the ability to sample gut antigens. Colony stimulating factor 1 controls the growth and differentiation of macrophages. Here the authors demonstrate that its blockade depletes gut macrophages and indirectly affects gut epithelial cell differentiation as the macrophages help maintain the Paneth and stem cells in intestinal crypts.
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      headline:The role of CSF1R-dependent macrophages in control of the intestinal stem-cell niche
      description:Colony-stimulating factor 1 (CSF1) controls the growth and differentiation of macrophages.CSF1R signaling has been implicated in the maintenance of the intestinal stem cell niche and differentiation of Paneth cells, but evidence of expression of CSF1R within the crypt is equivocal. Here we show that CSF1R-dependent macrophages influence intestinal epithelial differentiation and homeostasis. In the intestinal lamina propria CSF1R mRNA expression is restricted to macrophages which are intimately associated with the crypt epithelium, and is undetectable in Paneth cells. Macrophage ablation following CSF1R blockade affects Paneth cell differentiation and leads to a reduction of Lgr5+ intestinal stem cells. The disturbances to the crypt caused by macrophage depletion adversely affect the subsequent differentiation of intestinal epithelial cell lineages. Goblet cell density is enhanced, whereas the development of M cells in Peyer’s patches is impeded. We suggest that modification of the phenotype or abundance of macrophages in the gut wall alters the development of the intestinal epithelium and the ability to sample gut antigens. Colony stimulating factor 1 controls the growth and differentiation of macrophages. Here the authors demonstrate that its blockade depletes gut macrophages and indirectly affects gut epithelial cell differentiation as the macrophages help maintain the Paneth and stem cells in intestinal crypts.
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