IL-10 and IL-4 synergize with TNF-alpha to induce IL-1ra production by human neutrophils.
The anti-inflammatory properties of IL-4, IL-10, IL-13 and TGF-beta are associated with their ability to repress the production of pro-inflammatory cytokines and to favour the release of interleukin-1 receptor antagonist (IL-1ra). Here, we investigate their actions on activated human polymorphonuclear cells (PMN). IL-4 and TGF-beta were able to increase the production of IL-1ra, however only IL-4 were able to further increase IL-1ra production in the presence of LPS. When IL-1ra production by PMN was induced by tumour necrosis factor-alpha (TNF-alpha), IL-10 and IL-4 both amplified its release and its presence as a cell-associated form. In conclusion, IL-10 which was unable to induce IL-1ra by itself or to amplify the LPS-induced production by PMN, was able to increase its release when TNF-alpha, is the triggering signal. IL-4 was active in the different combinations tested; IL-13 and TGF-beta did not further modulate LPS- and TNF-alpha-induced IL-1ra production by PMN.
Marie
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Unité d'Immuno-Allergie, Institut Pasteur, Paris, France.
Pitton
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C
Fitting
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Cavaillon
J M
JM
D002478:Cells, Cultured; D004357:Drug Synergism; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D016753:Interleukin-10 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D011994:Recombinant Proteins / Q000494:pharmacology; D012016:Reference Values; D012795:Sialoglycoproteins / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011994:Recombinant Proteins; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4