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The Journal of Immunology, Vol 141, Issue 4 1180-1184, Copyright © 1988 by American Association of Immunologists
ARTICLES |
BY Rubin, SL Anderson, RM Lunn, NK Richardson, GR Hellermann, LJ Smith and LJ Old
Department of Lymphokine Biology, New York Blood Center 10021.
The treatment of cells with TNF or IFN results in the development of an antiviral state and in the induction of a common set of proteins with m.w. of 80,000, 67,000, and 56,000. The induction of the 80,000- and 56,000-Da proteins after TNF treatment is dependent on the synthesis of an intermediary protein, whereas the induction of the 67,000-Da protein appears to occur as a direct result of the TNF treatment. The effects of antibodies to IFN on the TNF-mediated effects have been evaluated and reveal that the incubation of TNF-treated cells with antibody to rIFN-beta 1 greatly reduces the antiviral effectiveness of the TNF treatment and blocks the ability of TNF to induce the 80,000-Da protein. Incubation with antibodies to either IFN-alpha or IFN-gamma failed to affect the TNF-mediated responses. Thus, the induction by TNF of each of the proteins is regulated differently and is mediated through both IFN-dependent and IFN-independent mechanisms.
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