Morita M, Saito H, Honjo T, Saito Y, Tsuruta S, Kim K M, Tanaka M, Mori K J, Mayumi M, Mikawa H
Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
Blood. 1991 Apr 15;77(8):1766-75.
Differentiation of a human eosinophilic leukemia cell line, EoL-1, induced by the culture supernatant of a human ATL cell line, HIL-3 (HIL-3 sup) was compared with differentiation induced by defined cytokines. HIL-3 sup induced EoL-1 cells to express eosinophilic granules and segmented nuclei after 6 to 9 days of incubation. HIL-3 sup also induced the expression of Fc epsilon receptor II (Fc epsilon RII/CD23) and an eosinophil differentiation antigen EO-1 mainly on eosinophilic granule (+) cells. Furthermore, HIL-3 sup induced EoL-1 cells to respond to an eosinophil chemotactic factor, platelet activating factor. HIL-3 cells express messenger RNA (mRNA) of interleukin-5 (IL-5), macrophage colony-stimulating factor (M-CSF), and IL-3 but not granulocyte CSF (G-CSF). Granulocyte-macrophage CSF (GM-CSF) and tumor necrosis factor-alpha (TNF-alpha) were detected in the HIL-3 sup. Recombinant IL-2 (rIL-2), rIL-3, rIL-4, rIL-5, rM-CSF, and rGM-CSF did not induce eosinophilic granules. rG-CSF induced a few eosinophilic granule (+) cells, and TNF-alpha, which did not induce eosinophilic granules by itself, enhanced the ability of G-CSF to induce them. However, G-CSF and TNF-alpha did not induce the expression of Fc epsilon RII and EO-1 antigen. Moreover, anti-G-CSF, anti-TNF-alpha, anti-GM-CSF, anti-IL-3, and anti-IL-5 antibodies did not suppress the effect of HIL-3 sup on the differentiation of EoL-1 cells. All the data suggest that HIL-3 sup contains an unidentified factor that induces differentiation of EoL-1 cells, and that EoL-1 cells and HIL-3 sup provide an important model for the examination of differentiation mechanisms and functions of eosinophils.
将人嗜酸性粒细胞白血病细胞系EoL-1由人成人T细胞白血病细胞系HIL-3的培养上清液（HIL-3 sup）诱导产生的分化，与由特定细胞因子诱导的分化进行了比较。在孵育6至9天后，HIL-3 sup诱导EoL-1细胞表达嗜酸性颗粒和分叶核。HIL-3 sup还主要在嗜酸性颗粒（+）细胞上诱导Fcε受体II（FcεRII/CD23）和嗜酸性粒细胞分化抗原EO-1的表达。此外，HIL-3 sup诱导EoL-1细胞对嗜酸性粒细胞趋化因子血小板活化因子产生反应。HIL-3细胞表达白细胞介素-5（IL-5）、巨噬细胞集落刺激因子（M-CSF）和IL-3的信使核糖核酸（mRNA），但不表达粒细胞集落刺激因子（G-CSF）。在HIL-3 sup中检测到粒细胞-巨噬细胞集落刺激因子（GM-CSF）和肿瘤坏死因子-α（TNF-α）。重组IL-2（rIL-2）、rIL-3、rIL-4、rIL-5、rM-CSF和rGM-CSF均未诱导嗜酸性颗粒的产生。rG-CSF诱导产生少数嗜酸性颗粒（+）细胞，而自身不诱导嗜酸性颗粒产生的TNF-α增强了G-CSF诱导嗜酸性颗粒产生的能力。然而，G-CSF和TNF-α并未诱导FcεRII和EO-1抗原的表达。此外，抗G-CSF、抗TNF-α、抗GM-CSF、抗IL-3和抗IL-5抗体均未抑制HIL-3 sup对EoL-1细胞分化的作用。所有数据表明，HIL-3 sup含有一种未鉴定的因子，可诱导EoL-1细胞分化，并且EoL-1细胞和HIL-3 sup为研究嗜酸性粒细胞的分化机制和功能提供了一个重要模型。
