Tumor necrosis factor stimulates interleukin-1 and prostaglandin E2 production in resting macrophages

doi:10.1016/0006-291X(86)90881-8

Biochemical and Biophysical Research Communications

Volume 136, Issue 1, 14 April 1986, Pages 94-101

https://doi.org/10.1016/0006-291X(86)90881-8 Get rights and content

Abstract

We have investigated the effect of tumor necrosis factor on the release of interleukin-1 and PGE₂ from murine resident peritoneal macrophages. Tumor necrosis factor causes an increase in the production of interleukin-1 and PGE₂ with a maximum induction for both noted at 5.9 × 10⁻⁸M. While indomethacin decreased tumor necrosis factor induced PGE₂ production, this cyclooxygenase inhibitor augmented tumor necrosis factor induced interleukin-1 production. Our data suggests that tumor necrosis factor may be an important immunopotentiating agent in addition to its previously described cytolytic and metabolic activities.

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Tumor necrosis factor stimulates interleukin-1 and prostaglandin E2 production in resting macrophages

Abstract

Biochem. Biophys. Res. Comm

N. Engl. J. Med

N. Engl. J. Med

Brit. J. Exp. Pathol

J. Exp. Med

J. Leuk. Biol

Science

Tumor necrosis factor stimulates interleukin-1 and prostaglandin E₂ production in resting macrophages