| First Author | Birnberg T | Year | 2008 |
| Journal | Immunity | Volume | 29 |
| Issue | 6 | Pages | 986-97 |
| PubMed ID | 19062318 | Mgi Jnum | J:142682 |
| Mgi Id | MGI:3821950 | Doi | 10.1016/j.immuni.2008.10.012 |
| Citation | Birnberg T, et al. (2008) Lack of conventional dendritic cells is compatible with normal development and T cell homeostasis, but causes myeloid proliferative syndrome. Immunity 29(6):986-97 |
| abstractText | Dendritic cells are critically involved in the promotion and regulation of T cell responses. Here, we report a mouse strain that lacks conventional CD11c(hi) dendritic cells (cDCs) because of constitutive cell-type specific expression of a suicide gene. As expected, cDC-less mice failed to mount effective T cell responses resulting in impaired viral clearance. In contrast, neither thymic negative selection nor T regulatory cell generation or T cell homeostasis were markedly affected. Unexpectedly, cDC-less mice developed a progressive myeloproliferative disorder characterized by prominent extramedullary hematopoiesis and increased serum amounts of the cytokine Flt3 ligand. Our data identify a critical role of cDCs in the control of steady-state hematopoiesis, revealing a feedback loop that links peripheral cDCs to myelogenesis through soluble growth factors, such as Flt3 ligand. |
