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输血诱导的免疫抑制中前列腺素的产生及抑制细胞的诱导

Prostaglandin production and suppressor cell induction in transfusion-induced immune suppression.

作者信息

Shelby J, Marushack M M, Nelson E W

出版信息

Transplantation. 1987 Jan;43(1):113-6. doi: 10.1097/00007890-198701000-00025.

Abstract

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.

摘要

使用了两种模型来研究前列腺素(PGE)在输血诱导的免疫抑制诱导阶段中的作用。首先,观察到术后同种异体第三方输血可延长主要组织相容性复合体(MHC)匹配的大鼠心脏同种异体移植的存活时间。此外,移植前抗原特异性同种异体输血可降低小鼠的移植物抗宿主(GVH)反应性。PGE合成抑制剂吲哚美辛,在给予输血的大鼠心脏受体或移植物抗宿主反应小鼠时,可阻断输血诱导的免疫抑制。抗PGE抗体对内源性PGE的中和作用也可阻断同种异体血液诱导的免疫抑制。同种异体血液诱导的脾脏抑制细胞下调了正常的GVH反应性,并且似乎是通过前列腺素依赖性途径产生的。

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