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Interleukin-4 (IL-4) inhibits secretion of IL-1 beta, tumor necrosis factor
alpha, and IL-6 by human monocytes
AA te Velde, RJ Huijbens, K Heije, JE de Vries and CG Figdor
Division of Immunology, The Netherlands Cancer Institute, Amsterdam.
Monocytes activated by lipopolysaccharide (LPS) and interferon gamma (IFN
gamma) rapidly secrete a number of monokines with different functional
properties. Interleukin-4 (IL-4), a T-cell derived cytokine, has been shown
to reduce the production of monokines with cytostatic activity for tumor
cells, chemotactic activity for monocytes, and factors that stimulate
thymocyte proliferation. This latter activity is mediated by a number of
monokines like IL-1, tumor necrosis factor alpha (TNF alpha), and IL-6. To
elucidate which cytokines produced by monocytes are controlled by IL-4, we
tested the effect of IL-4 on the secretion of IL-1 alpha, IL-1 beta, TNF
alpha, and IL-6 induced by LPS or IFN gamma. IL-4 was found to inhibit the
secretion of IL-1 beta and TNF alpha by activated monocytes almost 100%.
The secretion of IL-6 was found to be reduced 70% to 85% in the presence of
IL-4, whereas there was no effect on the secretion of IL-1 alpha (IL-1
alpha is mainly cell- associated). Time-course experiments demonstrate that
IL-4 reduces the secretion of monokines for a prolonged period of time
(greater than 40 hours). The reduced secretion of IL-1 beta and TNF alpha
was specifically induced by IL-4 because anti-IL-4 antiserum completely
restored normal monokine production. These data suggest that IL-4 plays a
role in the regulation of immune responses by reducing the production of
functionally important monokines.
Volume 76,
Issue 7,
pp. 1392-1397,
10/01/1990
Copyright © 1990 by The American Society of Hematology
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