Inhibition of AMP-activated protein kinase suppresses IL-2 expression through down-regulation of NF-AT and AP-1 activation in Jurkat T cells

Bong Sook Jhun, Jung Yeon Lee, Young Taek Oh, Ju Hie Lee, Wonchae Choe, Hyung Hwan Baik, Sung Soo Kim, Kyung Sik Yoon, Joohun Ha, Insug Kang

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

AMP-activated protein kinase (AMPK) is a key regulator of energy homeostasis and its activation during T cell receptor stimulation has recently been reported. In this study, we examined the role of AMPK in interleukin (IL)-2 production in T cells. Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKα1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. We then showed that AMPK inhibition reduced PMA/Io-induced IL-2 mRNA expression and IL-2 promoter activation. Moreover, inhibition of AMPK suppressed transcriptional activation of NF-AT and AP-1, but not NF-κB, in PMA/Io-activated Jurkat cells. Finally, we found that compound C inhibited PMA/Io-induced phosphorylation of p38, JNK, and GSK-3β but not of ERK. These results suggest that AMPK mediates IL-2 production by regulating NF-AT and AP-1activation during T cell stimulation.

Original languageEnglish (US)
Pages (from-to)986-992
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume351
Issue number4
DOIs
StatePublished - Dec 29 2006

Keywords

  • AMPK
  • AP-1
  • CD3
  • GSK-3
  • IL-2
  • Ionomycin
  • Jurkat cells
  • MAPK
  • NF-AT
  • PMA

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