AI Article Synopsis
- The study focuses on the role of the CSF1R receptor in the development and survival of mononuclear phagocytes (macrophages) in mammals.
- Researchers found that deleting a specific regulatory element, FIRE, in mice reduced CSF1R expression and disrupted macrophage development in certain tissues, leading to a lack of macrophages in various areas such as the brain and skin.
- Despite these changes, the mice appeared healthy and did not show any major developmental or neurological issues, making them useful for studying the functions of specific macrophage populations in adults.
Article Abstract
The proliferation, differentiation and survival of mononuclear phagocytes depend on signals from the receptor for macrophage colony-stimulating factor, CSF1R. The mammalian Csf1r locus contains a highly conserved super-enhancer, the fms-intronic regulatory element (FIRE). Here we show that genomic deletion of FIRE in mice selectively impacts CSF1R expression and tissue macrophage development in specific tissues. Deletion of FIRE ablates macrophage development from murine embryonic stem cells. Csf1r mice lack macrophages in the embryo, brain microglia and resident macrophages in the skin, kidney, heart and peritoneum. The homeostasis of other macrophage populations and monocytes is unaffected, but monocytes and their progenitors in bone marrow lack surface CSF1R. Finally, Csf1r mice are healthy and fertile without the growth, neurological or developmental abnormalities reported in Csf1r rodents. Csf1r mice thus provide a model to explore the homeostatic, physiological and immunological functions of tissue-specific macrophage populations in adult animals.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642117 | PMC |
| http://dx.doi.org/10.1038/s41467-019-11053-8 | DOI Listing |
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