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Release in Lipopolysaccharide-Stimulated Human Monocytes Through TGF-
1
* Experimental Medicine Unit and
Ludwig Institute for Cancer Research, Christian de Duve Institute of Cellular Pathology, and
Laboratory of Hematology, Université de Louvain, Brussels, Belgium
IL-9 is a Th2 cytokine that exerts pleiotropic activities on T
cells, B cells, mast cells, hematopoietic progenitors, and lung
epithelial cells, but no effect of this cytokine has been reported so
far on mononuclear phagocytes. Human blood monocytes preincubated with
IL-9 for 24 h before LPS or PMA stimulation exhibited a decreased
oxidative burst, even in the presence of IFN-
. The inhibitory effect
of IL-9 was specifically abolished by anti-hIL-9R mAb, and the
presence of IL-9 receptors was demonstrated on human blood monocytes by
FACS. IL-9 also down-regulated TNF-
and IL-10 release by
LPS-stimulated monocytes. In addition, IL-9 strongly up-regulated the
production of TGF-
1 by LPS-stimulated monocytes. The suppressive
effect of IL-9 on the respiratory burst and TNF- production in
LPS-stimulated monocytes was significantly inhibited by
anti-TGF-1, but not by anti-IL-10R mAb. Furthermore, IL-9
inhibited LPS-induced activation of extracellular signal-regulated
kinase 1/2 mitogen-activated protein kinases in monocytes through a
TGF--mediated induction of protein phosphatase activity. In
contrast, IL-4, which exerts a similar inhibitory effect on the
oxidative burst and TNF- release by monocytes, acts primarily
through a down-regulation of LPS receptors. Thus, IL-9 deactivates
LPS-stimulated blood mononuclear phagocytes, and the mechanism of
inhibition involves the potentiation of TGF-1 production and
extracellular signal-regulated kinase inhibition. These findings
highlight a new target cell for IL-9 and may account for the beneficial
activity of IL-9 in animal models of exaggerated inflammatory
response.
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