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Interleukin-13 (IL-13) induces IL-1 receptor antagonist gene expression and
protein synthesis in peripheral blood mononuclear cells: inhibition by an
IL-4 mutant protein
E Vannier, R de Waal Malefyt, A Salazar-Montes, JE de Vries and CA Dinarello
Department of Medicine, Tufts University of Medicine, Boston, Masachusetts
USA.
Interleukin-13 (IL-13) belongs to the IL-4 gene family. Like IL-4, IL- 13
induces IL-1 receptor antagonist (IL-1Ra) synthesis with no effect on
IL-1beta synthesis. We investigated whether IL-13 induces IL-1Ra synthesis
via a pathway similar to IL-4. In human peripheral blood mononuclear cells,
IL-13 (1 to 100 ng/mL alone induced IL-1Ra synthesis in a dose-dependent
manner. A single amino acid mutant form of IL-4 (hIL4.Yl24D) induced IL-1Ra
synthesis, acting as a partial agonist. However, hIL-4.Yl24D inhibited
IL-1Ra synthesis induced by either IL-4 or IL-13. IL-13 alone induced
accumulation of IL-1Ra mRNA. Furthermore, IL-13 reduced steady- state
levels for IL-1beta mRNA but enhanced those for IL-1Ra mRNA in cells
stimulated with lipopolysaccharide (LPS) or IL- 1alpha. Accordingly, IL-13
suppressed IL-1beta synthesis but enhanced IL-1Ra synthesis in these cells.
IL-13 reduced the stability of IL- 1beta mRNA (2.9 v 1.7 hours) but failed
to modify the stability of IL- 1Ra mRNA (2.7 v 2.5 hours). Moreover, IL-13
induced transcriptional activation of the IL-1Ra gene, but reduced IL-1beta
gene transcription. Our results suggest that the commonality between IL-13
and IL-4 in inducing IL-1Ra synthesis results from the engagement of a
subunit common to both receptors.
Volume 87,
Issue 8,
pp. 3307-3315,
04/15/1996
Copyright © 1996 by The American Society of Hematology
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