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• W2000492555 abstract "Abstract 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." @default.
• W2000492555 created "2016-06-24" @default.
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• W2000492555 date "2006-11-29" @default.
• W2000492555 modified "2023-10-15" @default.
• W2000492555 title "Prostaglandin I2 analogs inhibit Th1 and Th2 effector cytokine production by CD4 T cells" @default.
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• W2000492555 doi "https://doi.org/10.1189/jlb.0606375" @default.
• W2000492555 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17135575" @default.
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