IL-24 is Expressed by Rat and Human Macrophages

Recently, a number of interleukin-10 (IL-10) homologues, among them IL-24 formerly known as melanocyte differentiation factor-7 (mda-7), has been described. Since IL-10 is released by macrophages and plays an important role in the resolution of inflammatory processes, we hypothesized that IL-24 migh...

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Bibliographic Details
Published in:Immunobiology (1979) 2002-07, Vol.205 (3), p.321-334
Main Authors: Garn, Holger, Schmidt, Ansgar, Grau, Veronika, Stumpf, Sabine, Kaufmann, Andreas, Becker, Mike, Gemsa, Diethard, Siese, Anette
Format: Article
Language:English
Subjects:
Animals
Genes, Tumor Suppressor
Humans
Influenza A virus - metabolism
Interleukins - biosynthesis
Interleukins - genetics
Macrophages, Alveolar - metabolism
Monocytes - metabolism
Orthomyxoviridae Infections - metabolism
Rats
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Summary:Recently, a number of interleukin-10 (IL-10) homologues, among them IL-24 formerly known as melanocyte differentiation factor-7 (mda-7), has been described. Since IL-10 is released by macrophages and plays an important role in the resolution of inflammatory processes, we hypothesized that IL-24 might also be expressed in cells of the monocyte/macrophage lineage. We analyzed IL-24 expression on the mRNA and protein level in stimulated rat and human macrophages. In rat alveolar macrophages and NR8383 cells, IL-24 mRNA induction was observed following stimulation with LPS and IL-4 whereas TNF-a failed. Intracellular IL-24 protein was detected in unstimulated and IL-4 stimulated NR8383 cells. Also human blood monocytes showed a strong up-regulation of IL-24 mRNA following preparation which was enhanced by LPS and lowered by IL-10. Furthermore, infection of human monocytes with influenza A virus A/PR/8 caused an induction of IL-24 mRNA expression. In conclusion, our data show that IL-24 expression is induced in stimulated and infected rat and human macrophages, however, more insights into the functions of IL-24 are necessary to define its physiological relevance.
ISSN:0171-2985
1878-3279
DOI:10.1078/0171-2985-00135