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Prostaglandin E 2 modulates dendritic cell function via EP 2 and EP 4 receptor subtypes

Abstract : We have reported previously that PGE(2) inhibits dendritic cells (DC) functions. Because E prostanoid receptor (EPR) subtypes involved in this action are unknown, expression and functions of these receptors were examined in DC. Western blot and flow cytometry analyses showed that all EPRs were coexpressed in DC. In a dose-dependent manner, lipopolysaccharide (LPS) enhanced EP(2)R/EP(4)R but not EP(1)R/EP(3)R expressions. NS-398, a cyclooxygenase (COX)-2-selective inhibitor, suppressed LPS-enhanced EP(2)R/EP(4)R expression, suggesting that COX-2-issued prostaglandin E(2) (PGE(2)) modulates DC function through stimulation of specific EPR subtypes. Using selective agonists, we found that butaprost, an EP(2)R agonist, and PGE(1) alcohol, an EP(2)R and EP(2)R/EP(4)R agonist, inhibited major histocompatibility complex class II expression and enhanced interleukin-10 production from DC. However, no effect was observed with sulprostone and 17-phenyl-omega-trinor-PGE(2), selective agonists for EP(1)R and EP(1)R/EP(3)R, respectively. Treatment of DC with dibutyryl cyclic adenosine monophosphate (cAMP), an analog of cAMP, mimics PGE(2)-induced, inhibitory effects. Taken together, our data demonstrate that EP(2)R/EP(4)R are efficient for mediating PGE(2)-induced modulation of DC functions.
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https://www.hal.inserm.fr/inserm-02519507
Contributor : Christophe Grosset <>
Submitted on : Thursday, March 26, 2020 - 10:02:44 AM
Last modification on : Sunday, May 31, 2020 - 2:28:02 AM

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Hedi Harizi, Christophe Grosset, Norbert Gualde. Prostaglandin E 2 modulates dendritic cell function via EP 2 and EP 4 receptor subtypes. Journal of Leukocyte Biology, Society for Leukocyte Biology, 2003, 73 (6), pp.756-763. ⟨10.1189/jlb.1002483⟩. ⟨inserm-02519507⟩

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