Prostaglandin E(2) (PGE(2)) is known to inhibit in vitro T-cell responses to mitogenic and antigenic stimuli. Interaction of PGE(2) with a G protein-coupled receptor activates adenylyl cyclase, leading to cAMP formation and inhibition of interleukin-2 (IL-2) production and T-cell proliferation. Despite these effects, the application of PGE(2) as an anti-inflammatory agent has been compromised by its unfavorable pharmacodynamic and side-effect profile.
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