Maintaining cellular cAMP homeostasis is thus essential ( Raker et al., 2016). We conclude that PDE4B is a homeostatic regulator of cellular cAMP concentrations in DCs and may be a target for treating Th2-allergic asthma and other settings with low cellular cAMP concentrations.Ĭellular concentration of the second messenger 3′,5′-cyclic adenosine monophosphate (cyclic AMP, cAMP) can profoundly impact organismal physiology. Treatment of DCs that drive enhanced Th2 immunity with a PDE4B inhibitor ameliorated DC-induced helper T cell response. PDE4B expression is dynamic, falling and rising in a protein kinase A-dependent manner with decreased and increased cAMP concentrations, respectively. We found that phosphodiesterase 4B (PDE4B) is the primary phosphodiesterase expressed in DCs and that its expression is preferentially decreased in Gα s-depleted DCs. These mice spontaneously develop Th2-allergic asthma and their DCs have persistently lower cAMP levels. We have used a unique system-murine dendritic cells (DCs) with a DC-selective depletion of the heterotrimeric GTP binding protein Gα s-to address this issue. 2Department of Medicine, University of California, San Diego, La Jolla, CA, United StatesĬhronic decreases in the second messenger cyclic AMP (cAMP) occur in numerous settings, but how cells compensate for such decreases is unknown.1Department of Pharmacology, University of California, San Diego, La Jolla, CA, United States.Chinn 1 Cristina Salmerón 1 Jihyung Lee 2 Krishna Sriram 1 Eyal Raz 2 Paul A.
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