| First Author | Varga T | Year | 2013 |
| Journal | J Immunol | Volume | 191 |
| Issue | 11 | Pages | 5695-701 |
| PubMed ID | 24133167 | Mgi Jnum | J:207030 |
| Mgi Id | MGI:5554321 | Doi | 10.4049/jimmunol.1301445 |
| Citation | Varga T, et al. (2013) Tissue LyC6- macrophages are generated in the absence of circulating LyC6- monocytes and Nur77 in a model of muscle regeneration. J Immunol 191(11):5695-701 |
| abstractText | There are several open questions regarding the origin, development, and differentiation of subpopulations of monocytes, macrophages (MFs), and dendritic cells. It is a particularly intriguing question how circulating monocyte subsets develop and contribute to the generation of steady-state and inflammatory tissue MF pools and which transcriptional mechanisms contribute to these processes. In this study, we took advantage of a genetic model in which LyC6(-) circulating monocyte development is severely diminished due to the lack of the nuclear receptor, NUR77. We show that, in a mouse model of skeletal muscle injury and regeneration, the accumulation of leukocytes and the generation of LyC6(+) and LyC6(-) MF pools are intact in the absence of circulating LyC6(-) blood monocytes. These data suggest that NUR77, which is required for LyC6(-) blood monocyte development, is expressed but not critically required for LyC6(+) to LyC6(-) tissue MF specification. Moreover, these observations support a model according to which tissue macrophage subtype specification is distinct from that of circulating monocytes. Lastly, our data show that in the used sterile inflammation model tissue LyC6(-) MFs are derived from LyC6(+) cells. |
