Modulation of macrophage I-A expression: lack of effect of prostaglandins and glucocorticoids on macrophages that continuously express I-A.
The ability of prostaglandins, glucocorticoids and lipopolysaccharide to modulate I-A expression on macrophages that continuously or transiently express I-A was compared. We found that neither prostaglandins nor glucocorticoids affected I-A expression by macrophages that continuously expressed I-A. In contrast, prostaglandin E2 (PGE2) inhibited the lymphokine-induced maintenance of I-A on macrophages that transiently expressed I-A while glucocorticoids inhibited both the induction and expression of I-A. Lipopolysaccharide caused a loss in the expression of Class II molecules on macrophages that continuously expressed I-A by a prostaglandin-independent mechanism. The lack of effect of PGE2 and glucocorticoids may be related to our observation that continuous expression of I-A does not require its continued synthesis.
Vespa
L
L
Johnson
S C
SC
Aldrich
W A
WA
Zwilling
B S
BS
D000818:Animals; D001500:BCG Vaccine / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology*; D000949:Histocompatibility Antigens Class II / Q000032:analysis*; D006854:Hydrocortisone / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D008809:Mice, Inbred C3H; D011453:Prostaglandins / Q000494:pharmacology*
D001500:BCG Vaccine; D005938:Glucocorticoids; D000949:Histocompatibility Antigens Class II; D008070:Lipopolysaccharides; D011453:Prostaglandins; D003907:Dexamethasone; D006854:Hydrocortisone