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Characterization of a Monocyte Differentiation Factor Distinct From Gamma‐Interferon, Tumor Necrosis Factor, or G,M‐Colony‐Stimulating Factor That Regulates the Growth and Functional Capabilities of the U937 Monocytic Cell Line
Author(s) -
Clement Loran T.,
Roberts Robert L.,
Martin Audrey M.
Publication year - 1988
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.44.2.101
Subject(s) - biology , u937 cell , monocyte , tumor necrosis factor alpha , interferon gamma , cell culture , tumor necrosis factor α , interferon , growth factor , microbiology and biotechnology , immunology , cancer research , cytokine , biochemistry , genetics , receptor
We have analyzed the characteristics and cellular sources of the T cell‐derived lymphokines that affect the proliferation and the oxidative metabolic capabilities of the U937 monocytic cell line. Although gamma‐interferon (gIFN) and tumor necrosis factor‐alpha (TNFa) can, in high doses, inhibit the proliferation of U937 cells, the predominant antiproliferative factor produced by activated CD4+ and CD8+ T cells has a MW=45‐55 Kd, is resistant to heat treatment, and is distinct and independent from gIFN, TNFa, and GM‐CSF. The inhibitory effect of this lymphokine on U937 cell growth requires an 18‐24‐hr induction period; thereafter, this growth arrest persists for up to 5 d, even in the absence of the factor. The lymphokine responsible for inducing oxidative metabolic capabilities in U937 cells is also a non‐gIFN, heat‐resistant, 45‐55‐Kd factor secreted by CD4+ and CD8+ cells, and we postulate that this differentiation factor is identical to the factor responsible for inhibiting U937 growth. These data demonstrate the prominent role of T cell‐derived factors distinct from gIFN, TNFa, or GM‐CSF in regulating the growth and functional capabilities of monocyte‐lineage cells. Furthermore, the data suggest it may be appropriate to distinguish monocyte activation, in which cells at a given maturational stage develop a heightened ability to perform a particular function, from changes in the functional repertoire of cells acquired as a consequence of lymphokine‐induced differentiation.