title: Differentiation of a human eosinophilic leukemia cell line (EoL-1) by a human T-cell leukemia cell line (HIL-3)-derived factor.
abstract: 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.
authors.affiliation: Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Morita
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: T
authors.initials: T
authors.lastname: Honjo
authors.forename: Y
authors.initials: Y
authors.lastname: Saito
authors.forename: S
authors.initials: S
authors.lastname: Tsuruta
authors.forename: K M
authors.initials: KM
authors.lastname: Kim
authors.forename: M
authors.initials: M
authors.lastname: Tanaka
authors.forename: K J
authors.initials: KJ
authors.lastname: Mori
authors.forename: M
authors.initials: M
authors.lastname: Mayumi
authors.forename: H
authors.initials: H
authors.lastname: Mikawa
mesh_terms: D000906:Antibodies; D001483:Base Sequence; D002454:Cell Differentiation / Q000187:drug effects*; D002460:Cell Line; D016207:Cytokines / Q000276:immunology / Q000494:pharmacology* / Q000502:physiology; D003594:Cytoplasmic Granules / Q000187:drug effects / Q000648:ultrastructure; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D007377:Interleukin-3 / Q000235:genetics / Q000494:pharmacology*; D007700:Kinetics; D015472:Leukemia, Eosinophilic, Acute; D015458:Leukemia, T-Cell; D008854:Microscopy, Electron; D008969:Molecular Sequence Data; D015345:Oligonucleotide Probes; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D000906:Antibodies; D016207:Cytokines; D007377:Interleukin-3; D015345:Oligonucleotide Probes; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor