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GM‐1, a Clone of the Monoblastic Phagocyte U937 That Expresses a Large Respiratory Burst Capacity Upon Activation With Interferon‐γ
Author(s) -
Garotta Gianni,
Thelen Marcus,
Delia Domenico,
Kamber Markus,
Baggiolini Marco
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.49.3.294
Subject(s) - biology , phagocyte , respiratory burst , clone (java method) , immunology , interferon , interferon gamma , respiratory system , phagocytosis , virology , genetics , gene , cytokine , anatomy
The human cell line U937 was cloned and screened for the responsiveness to interferon‐γ (INF‐γ). The selected subclone, named GM‐1, expressed a high density of IFN‐γ receptors and showed HLA typing similar to that of the parental line but was devoid of the Y chromosome. GM‐1 cells display a promyeloid phenotype as revealed by flow cytometry using a panel of murine antibodies. Following treatment with IFN‐γ GM‐1 cells differentiated to a more mature monocyte stage and acquired the capacity to mount a respiratory burst. After treatment with differentiation promoters, such as phorbol 12‐myristate 13‐acetate (PMA), dimethyl sulfoxide (DMSO), and retinoic acid, GM‐1 showed a more limited respiratory burst capacity. Superoxide release in IFN‐γ‐activated cells was stimulated with f‐Met‐Leu‐Phe, C5a, or PMA. The development of the respiratory burst capacity was accompanied with the expression of cytochrome b 558 , a component of the phagocyte NADPH‐oxidase. GM‐1 cells are useful for the study of the effects of IFN‐γ on the respiratory burst. They are more sensitive and yield a more homogenous response to IFN‐γ than U937 cells. The phenotype of GM‐1 cells was stable for more than 5 years.