Modulation of human natural killer cell activity by pharmacological mediators.
We have studied the effects of various pharmacological mediators on human NK cell activity. Prostaglandin E2 (PGE2) inhibits NK cell activity in a dose-dependent fashion, whereas PGF2 alpha has no significant effect over the same concentration range. Histamine at high doses (10(-4) M) induced a small but significant inhibition of NK cell activity which was mimicked by both H1 and H2 specific histamine receptor agonists. Inhibition of endogenous prostaglandin production by indomethacin did not alter NK cell activity. Inhibition of NK activity by cAMP but not cGMP analogues, together with other data presented suggests that the mechanism of PGE2-induced inhibition of NK cell activity is not due to impairment of effector cell movement or effector: target cell interaction, but through the adenylate cyclase system which modulates the killing process.
D003994:Bucladesine / Q000494:pharmacology; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D003995:Dibutyryl Cyclic GMP / Q000494:pharmacology; D015237:Dinoprost; D015232:Dinoprostone; D004305:Dose-Response Relationship, Drug; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000187:drug effects*; D008761:Methylhistamines / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology
D008761:Methylhistamines; D011458:Prostaglandins E; D011460:Prostaglandins F; D003995:Dibutyryl Cyclic GMP; C025566:4-methylhistamine; D003994:Bucladesine; D006632:Histamine; D015237:Dinoprost; C026259:2-methylhistamine; D015232:Dinoprostone; D007213:Indomethacin