O'Keeffe Meredith, Fancke Ben, Hochrein Hubertus
Research Department, Bavarian Nordic GmbH, Martinsried, Germany.
Methods Mol Biol. 2010;595:187-93. doi: 10.1007/978-1-60761-421-0_12.
Mice lacking the ligand for Flt-3 (CD135) have a massive deficit of dendritic cells (DC) in all organs. This phenotype of FL (FL) knockout mice suggested that FL was the archetypal DC poietin in the steady state. However, FL knockout mice also have reduced numbers of common lymphoid progenitors (CLP) and common myeloid progenitors (CMP) so it is possible that FL deficiency may limit the ability of other growth factors to drive DC development by limiting the pool of progenitor cells available. We found that DC development could be driven from BM cells of FL knockout mice using the myeloid growth factor M-CSF. The M-CSF-driven DC (MDC) developed independently of FL and resembled the DC types present in the spleen in the steady state.
缺乏Flt-3(CD135)配体的小鼠在所有器官中都存在大量树突状细胞(DC)缺陷。Flt-3配体(FL)基因敲除小鼠的这种表型表明,FL是稳态下典型的DC生成素。然而,FL基因敲除小鼠的普通淋巴祖细胞(CLP)和普通髓系祖细胞(CMP)数量也减少,因此FL缺乏可能通过限制可用祖细胞池来限制其他生长因子驱动DC发育的能力。我们发现,使用髓系生长因子M-CSF可从FL基因敲除小鼠的骨髓细胞驱动DC发育。M-CSF驱动的DC(MDC)独立于FL发育,且类似于稳态下脾脏中存在的DC类型。