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Department of Microbiology, National Public Health Institute, Helsinki, Finland
IL-23 is a novel cytokine that promotes the proliferation of naive
and memory T cells and stimulates their IFN-
production. Besides
functional similarities, IL-23 bears structural resemblance to IL-12.
Biologically active IL-23 is a heterodimer whose p40 subunit is
identical to IL-12p40 while its p19 subunit is distantly related to
IL-12p35. In the present study we demonstrate that human
monocyte-derived macrophages are able to produce IL-23 in response to
virus infection. Sendai virus stimulates the expression of p19 and p40
mRNAs in macrophages. Furthermore, it enhances p35 mRNA expression and
the production of IL-12. Influenza A virus, in contrast, fails to
stimulate IL-12 or IL-23 expression in macrophages. IL-12 and IL-23
contribute to the IFN--inducing activity that cell culture
supernatant from Sendai virus-infected macrophages show in NK-92 cells.
The induction of IFN- production occurs in concert with IFN-
and IL-18, which are also secreted from the virus-infected cells. The
IFN--inducing activity is inhibited by IL-4, which down-regulates
the transcription of p19 and p40 genes
and the secretion of IFN-, IL-12, and IL-18. IFN-, in
contrast, up-regulates the p19 and p40 mRNA expression in Sendai virus
infection. Thus, IL-4 and IFN- serve as opposing factors in the
regulation of IFN--inducing cytokines, including IL-23, in
macrophages.
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