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Interferon-gamma enhances expression of cellular receptors for tumor necrosis factor.

Masafumi Tsujimoto, +2 more
- 01 Apr 1986 - 
- Vol. 136, Iss: 7, pp 2441-2444
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TLDR
Incubation of several human tumor cell lines with human interferon-gamma (IFN-Gamma) increased the specific binding of subsequently added 125I-labeled recombinant human tumor necrosis factor (TNF).
Abstract
Incubation of several human tumor cell lines with human interferon-gamma (IFN-gamma) increased the specific binding of subsequently added 125I-labeled recombinant human tumor necrosis factor (TNF). A similar increase in TNF binding was seen in murine L929 cells after incubation with murine IFN-gamma, but not after incubation with human IFN-gamma. Increased TNF binding to cells incubated with IFN-gamma was due to an increase in the number of TNF receptors, with no demonstrable change in binding affinity. In one out of two human cell lines tested, IFN-alpha and IFN-beta also produced increased TNF binding, albeit with a lower efficacy than IFN-gamma. A maximal increase in TNF binding was seen after about 6 to 12 hr of incubation with IFN. Increased TNF binding due to enhanced TNF receptor expression may contribute to the enhancement of TNF cytotoxicity seen in some tumor cell lines after INF treatment. Modulation of TNF receptor expression by IFN may also influence other biological activities of TNF.

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Interferon-γ: an overview of signals, mechanisms and functions

TL;DR: The current understanding of IFN‐γ ligand, receptor, ignal transduction, and cellular effects with a focus on macrophage responses and to a lesser extent, responses from other cell types that influence macrophages function during infection are reviewed.
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Cellular responses to interferon-gamma.

TL;DR: Much of the cellular response to IFN-gamma can be described in terms of a set of integrated molecular programs underlying well-defined physiological systems, for example the induction of efficient antigen processing for MHC-mediated antigen presentation, which play clearly defined roles in pathogen resistance.
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A cell-killing monoclonal antibody (anti-Fas) to a cell surface antigen co-downregulated with the receptor of tumor necrosis factor

TL;DR: It is suggested that the cell-killing activity of TNF is mediated by Fas antigen associated with the TNF-R, an mAb specific for a human cell surface component (termed anti-Fas mAb).
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Induction of manganous superoxide dismutase by tumor necrosis factor: possible protective mechanism.

TL;DR: TNF-alpha induced MnSOD mRNA in all cell lines and normal cells examined in vitro and in various organs of mice in vivo, which may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF- alpha and cycloheximide.
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Two tumor necrosis factor-binding proteins purified from human urine. Evidence for immunological cross-reactivity with cell surface tumor necrosis factor receptors.

TL;DR: The findings presented in this study are consistent with the notion that the urinary TNF-binding proteins constitute soluble forms of the two molecular species of the cell surface TNF receptors.
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