Suppression of Interleukin-2 Expression by Arachidonylethanolamide is Mediated by Down-regulation of NF-AT

  • Lee, Jung-Hee (Department of Biochemistry, College of Medicine, Inje University) ;
  • Park, Kyung-Ran (Department of Biochemistry, College of Medicine, Inje University) ;
  • Yea, Sung-Su (Department of Biochemistry, College of Medicine, Inje University)
  • Published : 2006.12.31

Abstract

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.

Keywords

References

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