Increased intracellular cyclic AMP levels block PKC-mediated T cell activation by inhibition of c-jun transcription

Ami Tamir, Noah Isakov

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Antigen binding to specific receptors on T cells (TCR) results in a rapid and transient phosphoinositide hydrolysis followed by activation of protein kinase C (PKC). Activators of adenylate cyclase or cell permeable cyclic AMP (cAMP) derivatives antagonize this effect and inhibit T cell activation by interfering with phosphoinositide turnover. We found that dibutyryl cAMP (dbcAMP) also affects intracellular event(s) remote from the phosphoinositide hydrolysis step. Thus, dbcAMP inhibits T cell activation by TPA + ionomycin which directly activate PKC and bypass the requirement for TCR perturbation. Under these conditions, dbcAMP was found to interfere with the TPA + ionomycin-mediated induction of c-jun encoding the JUN/AP-1 transcription factor. The data suggest that increased cAMP levels interfere with several activation steps in T cells including the induction of early activation genes possessing the consensus AP-1 recognition site.

Original languageEnglish
Pages (from-to)95-99
Number of pages5
JournalImmunology Letters
Volume27
Issue number2
DOIs
StatePublished - 1 Jan 1991

Keywords

  • AP-1
  • Cyclic AMP
  • PKC
  • T cell activation
  • fos
  • jun

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