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KMID : 1034820060020040223
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Molecular & Cellular Toxicology
2006 Volume.2 No. 4 p.223 ~ p.228
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Suppression of Interleukin-2 Expression by Arachidonylethanolamide is Mediated by Down-regulation of NF-AT
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Lee Jung-Hee
Park Kyung-Ran
Yea Sung-Su
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Abstract
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Several plant-derived cannabinoids and endogenous ligands for cannabinoid receptors such as 2-arachidonyl-glycerol have been known to inhibit interleukin-2 (IL-2) expression. In the present study, we utilized arachidonylethanolamide (AEA), a putative endogenous ligand for cannabinoid receptors, to determine whether AEA modulated the expression of IL-2. AEA inhibited phorbol 12-myristate 13-acetate (PMA) plus ionomycin (Io)-induced IL-2 protein secretion and mRNA expression in EL-4 mouse T-cells as determined by ELISA and RT-PCR, respectively. To further characterize the inhibitory mechanism of AEA at the transcriptional level, we performed promoter study for IL-2 gene in PMA/Io-stimulated EL-4 cells. AEA decreased the transcriptional activity of the nuclear factor of activated T-cells (NF-AT) as well as the IL-2 promoter activity. These results suggest that AEA suppresses IL-2 expression and that the inhibition is mediated, at least in part, through the down-regulation of NF-AT.
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KEYWORD
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Arachidonylethanolamide, Interleukin-2, Nuclear factor of activated T-cells
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