Interferon-alpha induces circulating tumor necrosis factor receptor p55 in
humans
H Tilg, W Vogel and CA Dinarello
Department of Medicine, University Hospital Innsbruck, Austria.
In the present studies we investigated the effect of interferon-alpha (IFN
alpha) on the release of the soluble (extracellular) form of the tumor
necrosis factor p55 receptor (TNFsRp55), because TNFsRp55 is a natural
antagonist of tumor necrosis factor (TNF)-induced inflammation and also
might be part of the antiinflammatory properties of IFN alpha. Plasma
levels of TNFsRp55 were measured by a specific radioimmunoassay in five
healthy volunteers and in five patients with chronic hepatitis C treated
with IFN alpha. Levels showed a significant increase after a single
injection of 5.0 million U IFN alpha in both healthy and hepatitis patient
groups. Peak values (3.5 to 4.5 ng/mL) were observed within 12 hours of
beginning treatment. Thereafter, levels promptly declined, reaching
baseline values within 24 hours. TNF alpha and C- reactive protein (CRP)
levels were below the detection limit in the same plasma samples. In
addition, IFN alpha suppressed significantly interleukin (IL)-1
alpha-induced TNF alpha protein synthesis by human peripheral blood
mononuclear cells. These results suggest that the antiinflammatory
properties of IFN alpha may be, in part, also due to the induction and/or
release of TNF soluble receptors and the suppression of TNF alpha
synthesis.
Volume 85,
Issue 2,
pp. 433-435,
01/15/1995
Copyright © 1995 by The American Society of Hematology
