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and IL-12 Induce IL-18 Receptor Gene Expression in Human NK and T Cells1
Department of Virology, National Public Health Institute, Helsinki, Finland
IL-18 is a proinflammatory cytokine that enhances innate and
specific Th1 immune responses. During microbial infections, IL-18 is
produced by activated macrophages. IL-18 exerts its effects in synergy
with IFN-
or IL-12 to induce IFN-
. Here we show that in human NK
and T cells IFN- and IL-12 strongly up-regulate mRNA expression of
the IL-18R components, accessory protein-like (AcPL) and IL-1R-related
protein (IL-1Rrp). In addition, IFN- enhanced the expression of
MyD88, an adaptor molecule involved in IL-18 signaling. Pretreatment of
T cells with IFN- or IL-12 enhanced IL-18-induced NF-
B activation
and sensitized the cells to respond to lower concentrations of IL-18.
AcPL and IL-1Rrp genes were strongly expressed in T cells polarized
with IL-12, whereas in IL-4-polarized cells these genes were expressed
at very low levels, indicating that AcPL and IL-1Rrp genes are
preferentially expressed in Th1 cells. In conclusion, the results
suggest that IFN- and IL-12 enhance innate as well as Th1 immune
response by inducing IL-18R expression.
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