These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Cyclic AMP synergy with Ca2+ for production of IFN-gamma by a cytolytic T cell clone is post-transcriptional.
    Author: Kaldy P, Schmitt-Verhulst AM.
    Journal: J Immunol; 1991 Apr 01; 146(7):2382-7. PubMed ID: 1848581.
    Abstract:
    PGE2 or products increasing the intracellular concentration of cAMP (cAMP)i) had opposite effects on the induction of IFN-gamma in a CTL clone, depending on the inducing agent. Activation via the TCR was inhibited, whereas induction by the Ca2+ ionophore ionomycin was enhanced in the presence of agents increasing (cAMP)i. Synergy between Ca2(+)-dependent and cAMP-dependent pathways was independent of the activation of protein kinase C (PKC). Low levels of IFN-gamma mRNA could be detected transiently after induction with ionomycin alone, whereas simultaneous induction with agents increasing (cAMP)i led to enhanced levels of IFN-gamma mRNA detectable up to 12 h. No IFN-gamma mRNA was detected when the CTL were activated with (cAMP)i-increasing agents alone or with PKC-activating agents such as PMA, suggesting that the transcriptional activation of the IFN-gamma gene was strictly dependent on the Ca2(+)-mediated and cyclosporin A-dependent event. Analyses of IFN-gamma mRNA transcription by "run-on" experiments on nuclei isolated after activation of the CTL indicated that the Ca2+ signal alone induces maximal transcription of the IFN-gamma gene, which is not increased by either PKC activation or an increase in cAMP, but that further processing or stabilization of the IFN-gamma precursor or mature mRNA require an additional signal, provided either via a PKC or via a PKA activation pathway. The data also suggest that a combination of inflammatory products leading to an increase in (Ca2+)i and to an increase in (cAMP)i may bypass the usually stringent control of T cell activation by the TCR/CD3 complex.
    [Abstract] [Full Text] [Related] [New Search]