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Published online before print June 3, 2004
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regulates IL-21 and IL-21R expression in human NK and T cells
Department of Microbiology, National Public Health Institute, Helsinki, Finland
1Correspondence: Department of Microbiology, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland. E-mail: mari.strengell{at}ktl.fi
Interleukin (IL)-21 is a T cell-derived cytokine that regulates innate and adaptive immune responses. IL-21 receptor (IL-21R), which is expressed in natural killer (NK) and T cells, is structurally homologous to IL-2Rß and IL-15R
. These receptors also share a common cytokine receptor 
-chain with IL-4, IL-7, and IL-9. Macrophage- or dendritic cell-derived interferon (IFN)-/ß is a key cytokine in regulation of NK and T cell functions. We demonstrate here that in addition to activating IFN- gene expression, IFN-/ß and IL-12 enhance the mRNA expression of IL-21 in activated human T cells. In addition, IFN-/ß enhanced T cell receptor stimulation-induced IL-21 and IFN- gene expression in resting T cells. The promoter analysis of IL-21 gene revealed a putative IFN- activation site element, which was found to bind signal transducer and activator of transcription 1 (STAT1), STAT2, STAT3, and STAT4 proteins in IFN-/ß-stimulated NK or T cell extracts. In contrast to IL-21 expression, IFN-/ß down-regulated IL-21R mRNA expression in NK and T cells. IFN-/ß-induced down-regulation of IL-21R expression resulted in reduced STAT3 phosphorylation and DNA binding after IL-21 stimulation. In conclusion, our results suggest a novel role for IFN-/ß in the regulation of IL-21 response.
Key Words: interferon • cytokine • lymphocyte • innate immunity
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