Prostaglandin E inhibits the production of human interleukin 2.
Prostaglandins of the E type specifically inhibited the production of interleukin 2 (IL-2) by normal human lymphocytes, whereas PG synthetase inhibitors such as indomethacin and fentiazac raised IL-2 production above normal levels. Removal of adherent cells from mononuclear cell populations also resulted in enhanced IL-2 production. The resultant nonadherent cell population lost sensitivity to the enhancement effect of PG synthetase inhibitors, suggesting that a PGE-producing adherent cell plays a major role in the regulation of IL-2.
D000085:Acetates / Q000494:pharmacology; D000527:Alprostadil; D002448:Cell Adhesion; D015237:Dinoprost; D015232:Dinoprostone; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007376:Interleukin-2 / Q000096:biosynthesis*; D008222:Lymphokines / Q000096:biosynthesis*; D008297:Male; D011454:Prostaglandins A / Q000494:pharmacology; D011458:Prostaglandins E / Q000096:biosynthesis / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology; D013844:Thiazoles / Q000494:pharmacology
D000085:Acetates; D007376:Interleukin-2; D008222:Lymphokines; D011454:Prostaglandins A; D011458:Prostaglandins E; D011460:Prostaglandins F; D013844:Thiazoles; C006124:fentiazac; D015237:Dinoprost; D000527:Alprostadil; C100008:prostaglandin A2; D015232:Dinoprostone; C100573:prostaglandin A1; C100006:prostaglandin F1; D007213:Indomethacin