Antisense cyclic adenosine 5'-monophosphate response element modulator up-regulates IL-2 in T cells from patients with systemic lupus erythematosus

J Immunol. 2002 Oct 15;169(8):4147-52. doi: 10.4049/jimmunol.169.8.4147.

Abstract

The cAMP response element modulator (CREM) has been shown to bind specifically to the -180 site of the IL-2 promoter in vitro. CREM protein is increased in T cells of patients with systemic lupus erythematosus (SLE), and it has been considered responsible for the decreased production of IL-2. In this work we show that transcriptional up-regulation is responsible for the increased CREM protein levels and that CREM binds to the IL-2 promoter in live SLE T cells. Suppression of the expression of CREM mRNA and protein by an antisense CREM plasmid, which was force expressed in SLE T cells by electroporation, resulted in decreased CREM protein binding to the IL-2 promoter and increased expression of IL-2 mRNA and protein. Our data demonstrate that antisense constructs can be used to effectively eliminate the expression of a transcriptional repressor. This approach can be used therapeutically in conditions where increased production of IL-2 is desired.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Cyclic AMP / physiology*
  • Cyclic AMP Response Element Modulator
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Down-Regulation / immunology
  • Female
  • Humans
  • Interleukin-2 / biosynthesis*
  • Interleukin-2 / genetics
  • Interleukin-2 / metabolism
  • Lupus Erythematosus, Systemic / genetics
  • Lupus Erythematosus, Systemic / immunology*
  • Male
  • Middle Aged
  • Oligonucleotides, Antisense / pharmacology*
  • Promoter Regions, Genetic / immunology
  • Protein Binding / genetics
  • Protein Binding / immunology
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / biosynthesis
  • Repressor Proteins*
  • Response Elements / physiology
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocyte Subsets / metabolism*
  • Transcription, Genetic / immunology
  • Transfection
  • Up-Regulation / immunology*

Substances

  • DNA-Binding Proteins
  • Interleukin-2
  • Oligonucleotides, Antisense
  • RNA, Messenger
  • Repressor Proteins
  • Cyclic AMP Response Element Modulator
  • Cyclic AMP