Modulation of human natural killer cell activity by pharmacological mediators
Hall, T.J.; Chen, S.H.; Brostoff, J.; Lydyard, P.M.
Clinical and Experimental Immunology 54(2): 493-500
1983
ISSN/ISBN: 0009-9104 PMID: 6317242 Document Number: 209460
The effects of various pharmacological mediators on human NK cell activity were studied. 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 [2-methylhistamine, 4-methylhistamine]. Inhibition of endogenous prostaglandin production by indomethacin did not alter NK cell activity. Inhibition of NK activity by the cAMP analog [dibutyryl cAMP] but not the cGMP analog [dibutyryl cGMP] 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.