Mak N K, Fung M C, Leung K N, Hapel A J
Experimental Haematology Group, John Curtin School of Medical Research, Australian National University, Canberra.
Cell Immunol. 1993 Aug;150(1):1-14. doi: 10.1006/cimm.1993.1173.
We have isolated a subclone (JCS) of the WEHI 3B myelomonocytic leukemia, which acquires the characteristics of mature macrophage lineage cells in the presence of PMA or noncytotoxic concentrations of TNF-alpha (600-1200 U/ml). JCS cells were compared with D+ and D- subclones of WEHI 3B. Unlike D+ cells, JCS cells did not produce differentiated granulocyte-macrophage colonies in the presence of postendotoxin serum or recombinant G-CSF. Stimulation with PMA or TNF-alpha reduced proliferation of JCS cells. TNF-alpha decreased the level of cell surface J11D antigen with concurrent increased expression of Mac-1 and FcR antigens and phagocytic activity. These TNF-alpha-mediated effects were enhanced by addition of IFN-gamma to the cultures. Furthermore, differentiation-inducing activity of PMA could be prevented using neutralizing anti-TNF-alpha antibodies. The results indicate that exogenous TNF-alpha can act as a differentiative agent for JCS cells and that endogenous TNF-alpha is the active substance when PMA is used to stimulate macrophage differentiation of JCS cells.
我们分离出了WEHI 3B骨髓单核细胞白血病的一个亚克隆（JCS），该亚克隆在存在佛波酯（PMA）或无细胞毒性浓度的肿瘤坏死因子-α（TNF-α，600 - 1200 U/ml）时获得成熟巨噬细胞谱系细胞的特征。将JCS细胞与WEHI 3B的D +和D -亚克隆进行比较。与D +细胞不同，JCS细胞在内毒素后血清或重组粒细胞集落刺激因子（G-CSF）存在的情况下不会产生分化的粒细胞-巨噬细胞集落。用PMA或TNF-α刺激可降低JCS细胞的增殖。TNF-α降低细胞表面J11D抗原水平，同时增加Mac-1和FcR抗原的表达以及吞噬活性。向培养物中添加干扰素-γ（IFN-γ）可增强这些TNF-α介导的效应。此外，使用中和抗TNF-α抗体可阻止PMA的诱导分化活性。结果表明，外源性TNF-α可作为JCS细胞的分化剂，并且当使用PMA刺激JCS细胞的巨噬细胞分化时，内源性TNF-α是活性物质。
