Differential effects of interferon-alpha and interferon-gamma on interleukin 1 secretion by monocytes

• Published in: The Journal of immunology (1950) Vol. 138; no. 8; pp. 2535 - 2540
• Main Authors: Gerrard, TL, Siegel, JP, Dyer, DR, Zoon, KC
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-04-1987; American Association of Immunologists
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immunobiology; Interferon Type I - pharmacology; Interferon-gamma - pharmacology; Interleukin-1 - secretion; Lipopolysaccharides - pharmacology; Lymphokines, interleukins ( function, expression); Monocytes - drug effects; Monocytes - secretion; Recombinant Proteins - pharmacology; Regulatory factors and their cellular receptors; Staphylococcus aureus - immunology; Stimulation, Chemical; Human; Cell culture; Monocyte; Alpha interferon; Leukocyte; Secretion; Interaction; Interleukin 1; Monokine; Interferon; Lymphokine; Gamma interferon
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.138.8.2535

We examined the effect of interferon (IFN)-alpha and IFN-gamma on the ability of human monocytes to secrete interleukin 1 (IL 1). IFN-alpha directly induced IL 1 secretion by monocytes. IFN-gamma did not induce any IL 1. IFN-gamma-stimulated monocyte supernatants were also negative for pyrogenic activity. However, IFN-gamma greatly enhanced the amount of IL 1 secreted when monocytes were stimulated by lipopolysaccharide or Staphylococcus aureus, even at concentrations which by themselves did not induce IL 1. IFN-alpha did not enhance IL 1 secretion induced by other stimuli. IFN-gamma enhanced IL 1 secretion by priming monocytes to be more sensitive to an IL 1-inducing stimulus. However, IFN-gamma does not enhance IL 1 induced by all stimuli, because there was no enhancement of IL 1 induced by PMA. Thus, IFN-alpha and IFN-gamma have very distinct roles in the induction and enhancement of IL 1 by monocytes.