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Suppression of T-cell responsiveness by inducible cAMP early repressor (ICER)

  1. Author:
    Bodor, J.
    Feigenbaum, L.
    Bodorova, J.
    Bare, C.
    Reitz, M. S.
    Gress, R. E.

  2. Author Address

    NCI, Expt Immunol Branch, Div Basic Sci, NIH, Bldg 10, Rm 4B14, 10 Ctr Dr, Bethesda, MD 20892 USA. NCI, Expt Immunol Branch, Div Basic Sci, NIH, Bethesda, MD 20892 USA. NCI, Transgen Mouse Model, Sci Applicat Int Corp, Frederick Canc Res & Dev Ctr, Ft Detrick, MD 21702 USA. Univ Maryland, Inst Human Virol, Baltimore, MD 21201 USA.
    1. Year: 2001
  2. Journal: Journal of Leukocyte Biology
    1. 69
    2. 6
    3. Pages: 1053-1059
  4. Type of Article: Article
  1. Abstract:

    Depending on the: nature of the costimulation of T lymphocytes, expression of regulatory cytokines slid chemokines is either susceptible or resistant to cyclic AMP (cAMP)-mediated inhibition. Our data show that cAMP-mediated inhibition of endogenously expressed cytokines, which is characteristic for T helper (Th) 1- and Th 2-like phenotypes, correlates with the induction of a potent transcriptional repressor, inducible cAMP early repressor (ICER), in both subsets of T cells activated under conditions of suboptimal interleukin-2 (IL-2) expression. Importantly, Th-specific expression of certain chemokines is also susceptible to cAMP-mediated transcriptional attenuation. To determine whether ICER per se, rather than forskolin- mediated elevation of intracellular cAMP, is responsible for the observed inhibitory effect, we generated transgenic mice expressing ICER under the control of a lymphocyte-specific lck promoter. On stimulation, transgenic thymocytes overexpressing ICER exhibited reduced levels of IL-2 and interferon (IFN)- gamma and failed to express the macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta genes. Splenic T cells from ICER- transgenic mice showed a defect in proliferation and lacked a mixed lymphocyte reaction response., implying that ICER- mediated inhibition of cytokine and chemokine expression might play an important role in T-cell inactivation.

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