| First Author | Lund H | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 5 | Pages | 1-7 |
| PubMed ID | 29662171 | Mgi Jnum | J:282382 |
| Mgi Id | MGI:6380763 | Doi | 10.1038/s41590-018-0091-5 |
| Citation | Lund H, et al. (2018) Fatal demyelinating disease is induced by monocyte-derived macrophages in the absence of TGF-beta signaling. Nat Immunol 19(5):1-7 |
| abstractText | The cytokine transforming growth factor-beta (TGF-beta) regulates the development and homeostasis of several tissue-resident macrophage populations, including microglia. TGF-beta is not critical for microglia survival but is required for the maintenance of the microglia-specific homeostatic gene signature(1,2). Under defined host conditions, circulating monocytes can compete for the microglial niche and give rise to long-lived monocyte-derived macrophages residing in the central nervous system (CNS)(3-5). Whether monocytes require TGF-beta for colonization of the microglial niche and maintenance of CNS integrity is unknown. We found that abrogation of TGF-beta signaling in CX3CR1(+) monocyte-derived macrophages led to rapid onset of a progressive and fatal demyelinating motor disease characterized by myelin-laden giant macrophages throughout the spinal cord. Tgfbr2-deficient macrophages were characterized by high expression of genes encoding proteins involved in antigen presentation, inflammation and phagocytosis. TGF-beta is thus crucial for the functional integration of monocytes into the CNS microenvironment. |
