Cornish J, Barabas A Z, Lannigan R, Rozing J
Department of Pathology, University of Calgary, Alberta, Canada.
Br J Exp Pathol. 1989 Oct;70(5):505-13.
In this study, the functional properties of the cells involved in the immunoregulation of Heymann nephritis (HN) have been investigated. HN is a disease model in the rat where the pathology closely resembles membranous glomerulonephropathy (MGN) in man. This autoimmune model is induced by injection of renal tubular antigen (RTA) incorporated in Freund's complete adjuvant (FCA). The strong B cell and plasma cell response in the chronic phase of HN, as determined by cell marker analyses, is predominantly antigen-non-specific. The secondary response pattern found was not only to RTA upon repeated immunization, but also to non-related antigen (SRBC). Although cell marker studies have indicated no major quantitative changes in the T cell population throughout the development of HN, a severe deregulation of the cellular immune response is observed especially during the induction period of HN. This was shown by a strong decrease of the mitogen-induced proliferative response and IL-2 production. This phenomenon is caused by both defective cellular components and inhibitory serological factors. Finally, in the chronic phase, these aberrations gradually return to normal.
在本研究中，对参与海曼肾炎（HN）免疫调节的细胞的功能特性进行了研究。HN是大鼠中的一种疾病模型，其病理与人类膜性肾小球肾炎（MGN）极为相似。这种自身免疫模型是通过注射掺入弗氏完全佐剂（FCA）中的肾小管抗原（RTA）诱导产生的。通过细胞标志物分析确定，在HN慢性期强烈的B细胞和浆细胞反应主要是非抗原特异性的。发现的二次反应模式不仅在重复免疫时针对RTA，而且针对非相关抗原（SRBC）。尽管细胞标志物研究表明在HN整个发展过程中T细胞群体没有重大的数量变化，但尤其是在HN诱导期观察到细胞免疫反应严重失调。这表现为丝裂原诱导的增殖反应和IL-2产生的强烈下降。这种现象是由有缺陷的细胞成分和抑制性血清学因素共同引起的。最后，在慢性期，这些异常逐渐恢复正常。
