Journal ArticleDOI
A cytokine network in human diploid fibroblasts: interactions of beta-interferons, tumor necrosis factor, platelet-derived growth factor, and interleukin-1.
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TLDR
It is demonstrated that the expression of the antiviral action of TNF can be enhanced by prior exposure of FS-4 cells to trace amounts of IFN-beta 1, and a complex network of interactions that involves the endogenous production of IFn-beta 2 is triggered by several growth-modulatory cytokines.Abstract:
Earlier studies demonstrated the induction of beta 2-interferon (IFN-beta 2) in human diploid fibroblasts (FS-4 strain) exposed to tumor necrosis factor (TNF). These studies suggested that IFN-beta 2 mediates an antiviral effect in TNF-treated cells and exerts a feedback inhibition of the mitogenic effect of TNF. Here we demonstrate that the expression of the antiviral action of TNF can be enhanced by prior exposure of FS-4 cells to trace amounts of IFN-beta 1. IFN-beta 1, at a higher concentration, can directly increase the expression of IFN-beta 2. Exposure of cells to TNF enhanced IFN-beta 2 (but not IFN-beta 1) mRNA expression in response to poly(I).poly(C), an IFN inducer which is also known to stimulate FS-4 cell growth. Platelet-derived growth factor and interleukin-1 also led to the increased expression of IFN-beta 2. However, platelet-derived growth factor and interleukin-1 could override the antiviral effect of TNF and also that of exogenously added IFN-beta 1. Our data suggest that a complex network of interactions that involves the endogenous production of IFN-beta 2 is triggered by several growth-modulatory cytokines. Cellular homeostasis is likely to represent a balance between the induction of IFN-beta 2 by these cytokines and their ability to override the inhibitory actions of IFN-beta 2.read more
Citations
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Interleukin-6 and the acute phase response
TL;DR: Systemic reaction characterized by fever, leukocytosis, increase in erythrocyte sedimentation rate, increases in LeucocyTosis secretion of ACTH and glucocorticoids, and by dramatic changes in the concentration of some plasma ,l' proteins.
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Interleukin-1 and interleukin-1 antagonism.
TL;DR: The recent cloning of a naturally occurring IL-1 receptor antagonist (IL-1ra) has opened new experimental and clinical approaches and reduced the severity of diseases such as hemodynamic shock, lethal sepsis, inflammatory bowel disease, experimental arthritis, and the spontaneous proliferation of human leukemic cells.
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Interferon beta 2/B-cell stimulatory factor type 2 shares identity with monocyte-derived hepatocyte-stimulating factor and regulates the major acute phase protein response in liver cells
TL;DR: It is demonstrated that monocyte-derived hepatocyte-stimulating factor and IFN-beta 2 share immunological and functional identity and that IFN -beta 2, also known as B-cell stimulatory factor and hybridoma plasmacytoma growth factor, has the hepatocyte as a major physiologic target and thereby is essential in controlling the hepatic acute phase response.
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Activation of interleukin-6 gene expression through the NF-kappa B transcription factor.
TL;DR: NF-kappa B is an important mediator for activation of the IL-6 gene by a variety of IL- 6 inducers in both U-937 and HeLa cells and that alternative inducible enhancer elements contribute in a cell-specific manner to IL-8 gene induction.
Book ChapterDOI
Interleukin-1 and its biologically related cytokines.
TL;DR: Interleukin-1 (IL-1) and tumor necrosis factor (TNF) participate in self-augmentation induction mechanisms in cultured cells stimulated with viruses, bacterial toxins, and active complement components, and of immune complex.
References
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Journal ArticleDOI
Tumor necrosis factor (cachectin) is an endogenous pyrogen and induces production of interleukin 1
Charles A. Dinarello,Joseph G. Cannon,Sheldon M. Wolff,H A Bernheim,Bruce Beutler,Anthony Cerami,Irene S. Figari,Michael A. Palladino,O'connor John +8 more
TL;DR: These studies show that TNF (cachectin) is another endogenous pyrogen which, like IL-1 and IFN-alpha, directly stimulate hypothalamic PGE2 synthesis and is an endogenous inducer ofIL-1.
Book
The Interferon System
TL;DR: From the combination of knowledge and actions, someone can improve their skill and ability and this will lead them to live and work much better.
Journal ArticleDOI
Tumor necrosis factor/cachectin interacts with endothelial cell receptors to induce release of interleukin 1.
TL;DR: Data indicate that TNF can bind specifically to endothelium and initiate a cascade of inflammatory and coagulant events on the vessel surface potentially central to the host response to neoplasia and sepsis.
Journal ArticleDOI
Fibroblast Growth Enhancing Activity of Tumor Necrosis Factor and Its Relationship to Other Polypeptide Growth Factors
Jan Vilcek,Vito J. Palombella,D. Henriksen-Destefano,C Swenson,Rena Feinman,M Hirai,Masafumi Tsujimoto +6 more
TL;DR: It is shown that highly purified E. coli-derived recombinant human TNF stimulated the growth of human FS- 4 diploid fibroblasts, and that the cytotoxic and cytostatic actions of TNF may be the result of an anomalous growth signal transduction in neoplastic cells lacking the constraints of normal growth control mechanisms.
Journal ArticleDOI
Induction of β2-interferon by tumor necrosis factor: A homeostatic mechanism in the control of cell proliferation
TL;DR: It is demonstrated that purified E. coli-derived recombinant human TNF inhibits encephalomyocarditis virus replication in "aged" human fibroblasts, suggesting that IFN-beta 2 has biological functions distinct from the other interferons.