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Differentiation of a human eosinophilic leukemia cell line (EoL-1) by a human T-cell leukemia cell line (HIL-3)-derived factor
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- M Morita
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- H Saito
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- T Honjo
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- Y Saito
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- S Tsuruta
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- KM Kim
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- M Tanaka
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- KJ Mori
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- M Mayumi
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
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- H Mikawa
- Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
Description
<jats:title>Abstract</jats:title> <jats:p>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.</jats:p>
Journal
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- Blood
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Blood 77 (8), 1766-1775, 1991-04-15
American Society of Hematology
