Litwin A, Adams L E, Levy R, Cline S, Hess E V
Immunology. 1971 May;20(5):755-66.
Experimental glomerulonephritis (EGN) was produced in Sprague-Dawley rats with a single intradermal injection of a renal tubular fraction called Fx1A. Presence of disease was confirmed by proteinuria and by light and electron microscopic changes. This antigen and also the non-nephritogenic antigen, Fx1B, were used to study cellular immunity in nephritic and three groups of control rats. 64 per cent (9/14) of the Fx1A immunized rats gave delayed hypersensitivity skin tests to Fx1A. The difference between the experimental and the three control groups was highly significant. Peripheral blood lymphocyte culture responses to Fx1A, Fx1B, phytohaemagglutinin-P, were studied in the nephritic and control groups. 77 per cent (10/13) of Fx1A immunized animals showed stimulation of their lymphocyte cultures with Fx1A. None of the control groups showed any significant stimulation. These experiments have demonstrated cellular immunity in EGN and support the possibility that these mechanisms may play a role in the production of this disease.
通过在斯普拉格-道利大鼠皮内单次注射一种名为Fx1A的肾小管成分来诱发实验性肾小球肾炎（EGN）。通过蛋白尿以及光镜和电镜变化来确认疾病的存在。使用这种抗原以及非致肾炎抗原Fx1B来研究患肾炎大鼠和三组对照大鼠的细胞免疫。64%（9/14）的经Fx1A免疫的大鼠对Fx1A进行迟发型超敏皮肤试验呈阳性。实验组与三个对照组之间的差异非常显著。在患肾炎组和对照组中研究了外周血淋巴细胞对Fx1A、Fx1B、植物血凝素-P的培养反应。77%（10/13）的经Fx1A免疫的动物其淋巴细胞培养物受到Fx1A刺激。对照组均未显示出任何显著刺激。这些实验证明了EGN中的细胞免疫，并支持这些机制可能在该疾病发生中起作用的可能性。
