Transcriptional regulation of the interleukin 2 gene by glucocorticoid hormones. Role of steroid receptor and antigen-responsive 5'-flanking sequences

J Biol Chem. 1990 May 15;265(14):8075-80.

Abstract

Dexamethasone treatment of the Jurkat T77 cell clone inhibited the enhancing effect of 12-O-tetradecanoylporbol-13-acetate (TPA) and the calcium ionophore A23187 on the interleukin 2 (IL2) mRNA levels and gene transcription from intact nuclei. Dexamethasone treatment of Jurkat T77 cells inhibited the TPA/A23187-dependent activation of the transcription from the transfected pIL2CAT, containing 600 base pairs of the genomic sequences upstream of the coding region of IL2 gene, including the TPA/calcium responsive cis-regulatory elements and promoter sequences, driving the expression of the chloramphenicol acetyltransferase (CAT) gene. Transfection of either Jurkat T77 cell clone or glucocorticoid-resistant Jurkat cells with a human glucocorticoid receptor cDNA under the transcriptional control of the Rous sarcoma virus long terminal repeat (LTR) (pRShGR alpha) significantly increased or induced, respectively, the dexamethasone-mediated inhibition of the TPA/A23187-dependent expression of pIL2-CAT as well as the enhancing effect on the expression of the cotransfected CAT gene under the control of the mouse mammary tumor virus LTR, as a marker of glucocorticoid receptor action. This suggests a role for the glucocorticoid receptor in mediating the dexamethasone action on IL2 gene expression. To study the cis-regulatory sequence specificity of the dexamethasone-induced interference with the TPA/A23187-mediated T cell activating signals, we studied the effect of the hormone on the regulatory elements contained in the Rous sarcoma virus and human T lymphotropic virus 1 long terminal repeats and the SV40 promoter, which are known to be transcriptionally enhanced by those activating agents. Dexamethasone was unable to interfere with the TPA/A23187-mediated enhancement of these cis-regulatory elements, suggesting that the hormone effect is specific for IL-2 gene sequences. Our data suggest that the dexamethasone-mediated transcriptional inhibition of the IL2 gene is mediated by an interference with the protein kinase C and calcium-mediated trans-activation of the antigen-responsive and T cell-specific elements lying in the 5'-flanking region of the gene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Avian Sarcoma Viruses / genetics
  • Calcimycin / pharmacology
  • Cell Nucleus / metabolism
  • Chloramphenicol O-Acetyltransferase / genetics
  • DNA, Recombinant
  • Dexamethasone / pharmacology*
  • Gene Expression Regulation / drug effects*
  • Human T-lymphotropic virus 1 / genetics
  • Humans
  • Hylobates
  • Interleukin-2 / genetics*
  • Mammary Tumor Virus, Mouse / genetics
  • Mice
  • Promoter Regions, Genetic
  • RNA, Messenger / metabolism
  • Receptors, Glucocorticoid / physiology
  • Regulatory Sequences, Nucleic Acid
  • Repetitive Sequences, Nucleic Acid
  • Simian virus 40 / genetics
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic / drug effects*
  • Transfection
  • Tumor Cells, Cultured

Substances

  • DNA, Recombinant
  • Interleukin-2
  • RNA, Messenger
  • Receptors, Glucocorticoid
  • Calcimycin
  • Dexamethasone
  • Chloramphenicol O-Acetyltransferase
  • Tetradecanoylphorbol Acetate