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自体免疫复合物肾炎的控制。I. 在T细胞致敏情况下对疾病的抑制。

Control of autologous immune complex nephritis. I. Suppression of the disease in the presence of T cell sensitization.

作者信息

Harmon W E, Grupe W E, Parkman R

出版信息

J Immunol. 1980 Mar;124(3):1034-8.

PMID:6444644
Abstract

Pretreatment of Lewis and Sprague-Dawley rats with the nephritogenic antigen, Fx1A, in incomplete Freund's adjuvant (IFA) reduced the incidence of autologous immune complex nephritis in rats subsequently challenged with Fx1A in complete Freund's adjuvant (CFA). The suppression was evidenced by a decrease in antibody production, in glomerular deposition of immunoglobulins, and in the incidence of proteinuria, and it was antigen specific. In vitro blastogenesis to Fx1A of lymphocytes from Fx1A-IFA-pretreated animals was normal. Rats pretreated with Fx1A-IFA initially developed a normal antibody response after challenge with Fx1A-CFA, but the response was not sustained. These results indicate that the Fx1A-IFA-induced suppressor mechanism does not inhibit sensitization, but rather modifies specific antibody production.

摘要

用致肾炎抗原Fx1A加不完全弗氏佐剂(IFA)对Lewis大鼠和Sprague-Dawley大鼠进行预处理,可降低随后用完全弗氏佐剂(CFA)中的Fx1A攻击的大鼠自体免疫复合物肾炎的发病率。这种抑制作用表现为抗体产生减少、免疫球蛋白在肾小球的沉积减少以及蛋白尿发病率降低,并且具有抗原特异性。来自经Fx1A-IFA预处理动物的淋巴细胞对Fx1A的体外母细胞化反应正常。经Fx1A-IFA预处理的大鼠在用Fx1A-CFA攻击后最初产生正常的抗体反应,但这种反应不能持续。这些结果表明,Fx1A-IFA诱导的抑制机制并不抑制致敏作用,而是改变特异性抗体的产生。

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