Prostaglandin production and suppressor cell induction in transfusion-induced immune suppression.
Two models were used to examine the role of prostaglandin (PGE) in the inductive phase of transfusion-induced suppression. First, it was observed that post-operative allogeneic third-party blood transfusion resulted in prolonged major histocompatibility complex (MHC)-compatible rat heart allograft survival. Additionally, pretransplant antigen-specific allogeneic transfusion decreased graft-versus-host (GVH) reactivity in mice. An inhibitor of PGE synthesis, indomethacin, blocked transfusion-induced suppression when it was administered to either transfused rat heart recipients, or graft-versus-host responder mice. Neutralization of endogenous PGE by anti-PGE antibody also blocked allogeneic blood induced suppression. Allogeneic-blood-induced splenic suppressor cells down-regulated normal GVH responsiveness, and appeared to be generated via a prostaglandin-dependent pathway.
D000818:Animals; D001803:Blood Transfusion; D006085:Graft Survival; D006087:Graft vs Host Reaction; D016027:Heart Transplantation; D007165:Immunosuppression Therapy; D007213:Indomethacin / Q000494:pharmacology; D051379:Mice; D011458:Prostaglandins E / Q000096:biosynthesis*; D051381:Rats; D013154:Spleen / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D011458:Prostaglandins E; D007213:Indomethacin