Inhibition of interleukin 2 production by prostaglandin E2 is not absolute but depends on the strength of the stimulating signal.
In view of the eminently important role of interleukin-2 (IL-2) in T-cell responses, and in view of reports about immune stimulatory effects of PGE2, we reinvestigated the question whether PGE2 inhibits IL-2 production. It was found that PGE2 does not inhibit IL-2 production in murine spleen cell cultures after optimal stimulation (5 micrograms/ml concanavalin A) but does inhibit at suboptimal stimulation conditions. The failure of PGE2 to inhibit IL-2 production at optimal concanavalin A concentration was demonstrated by two independent IL-2 assays namely by the co-stimulator assay and by the proliferation of IL-2-dependent T-cell clone W-2. Our observations indicated that the inhibitory effect of PGE2 depends on the strength of the stimulating signal. IL-2 production in cultures with 5 micrograms/ml concanavalin A was also not suppressed by PGE1, by prostaglandin D2, thromboxane B2 (T X B2), and prostaglandin F2.
D000818:Animals; D003208:Concanavalin A / Q000494:pharmacology; D003864:Depression, Chemical; D015232:Dinoprostone; D004305:Dose-Response Relationship, Drug; D007376:Interleukin-2 / Q000096:biosynthesis*; D008297:Male; D051379:Mice; D011458:Prostaglandins E / Q000494:pharmacology*; D013154:Spleen / Q000166:cytology
D007376:Interleukin-2; D011458:Prostaglandins E; D003208:Concanavalin A; D015232:Dinoprostone