Prostaglandin I2 analogs inhibit Th1 and Th2 effector cytokine production by CD4 T cells

DOI PDF Web Site 被引用文献7件
  • Weisong Zhou
    Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine , Nashville, Tennessee , USA
  • Timothy S Blackwell
    Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine , Nashville, Tennessee , USA
  • Kasia Goleniewska
    Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine , Nashville, Tennessee , USA
  • Jamye F O’Neal
    Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine , Nashville, Tennessee , USA
  • Garret A FitzGerald
    Department of Medicine and Pharmacology, University of Pennsylvania , Philadelphia, Pennsylvania , USA
  • Margaret Lucitt
    Department of Medicine and Pharmacology, University of Pennsylvania , Philadelphia, Pennsylvania , USA
  • Richard M Breyer
    Department of Pharmacology, Vanderbilt University School of Medicine , Nashville, Tennessee , USA
  • R Stokes Peebles
    Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine , Nashville, Tennessee , USA

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公開日
2006-11-29
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.1189/jlb.0606375
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title><jats:p>An anti-inflammatory effect of PGI2 has been suggested by increased inflammation in mice that are deficient in the PGI2 receptor (IP) or in respiratory syncytial viral- or OVA-induced CD4 T cell-associated responses. To determine the mechanism of the anti-inflammatory effect, we hypothesized that PGI2 analogs inhibit CD4 T cell effector cytokine production. To test this hypothesis, we activated purified CD4 T cells with anti-CD3 and anti-CD28 antibodies under Th1 and Th2 polarizing conditions for 4 days and restimulated the T cells with anti-CD3 in the presence of PGI2 analogs for 2 days. We found that PGI2 analogs (cicaprost and iloprost) inhibited the production of Th1 cytokines (IFN-γ) and Th2 cytokines (IL-4, IL-10, and IL-13) in a dose-dependent pattern. The inhibitory effect was partially dependent on the IP receptor signaling and was correlated with elevated intracellular cAMP and down-regulated NF-κB activity. Pretreatment of the CD4 T cells with 8-bromoadenosine-3′,5′-cyclic monophosphorothioate, Rp-isomer, to inhibit a key signaling molecule in the cAMP pathway, protein kinase A (PKA), attenuated the suppressive effect of PGI2 analogs significantly, suggesting that PKA, in part, mediates the inhibition of the cytokine production. These data indicate that PGI2 analogs have an immune-suppressive effect on previously activated and differentiated CD4 T cells in vitro and suggest that PGI2 may have a similar function in vivo.</jats:p>

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