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):495-504.
Immunoregulation was examined in rats with Heymann nephritis (HN), an established model of membranous glomerulonephropathy (MGN). There is little known of the cellular immune events for the induction and maintenance of the autoimmune response in HN. The cell marker studies utilized fluorescein (FITC)-labelled monoclonal antibodies directed to B cells (Mark-I), and T cell subsets: pan T (ER-I), helper/inducer T (ER-2) and suppressor/cytotoxic T (ER-3). Lymphoid subsets were compared in spleen, lymph nodes, peripheral blood and bone marrow, of normal and diseased rats. Animals were investigated during the induction and chronic phases of disease. The induction of HN was associated with an early, significant, but transient increase of the non-specific myeloid component of the defence system. Subsequently, a significant increase was seen in the number of cells of the B lymphocyte lineage in HN animals, which coincided well with the overall increased humoral immune responsiveness. No alterations in the T lymphocyte subsets were noted during the development of this experimental autoimmune disease.
在海曼肾炎（HN）大鼠中研究了免疫调节，HN是膜性肾小球肾炎（MGN）的既定模型。对于HN中自身免疫反应的诱导和维持所涉及的细胞免疫事件知之甚少。细胞标志物研究使用了针对B细胞（标记-I）以及T细胞亚群的荧光素（FITC）标记单克隆抗体：全T细胞（ER-I）、辅助/诱导性T细胞（ER-2）和抑制/细胞毒性T细胞（ER-3）。比较了正常大鼠和患病大鼠脾脏、淋巴结、外周血和骨髓中的淋巴细胞亚群。在疾病的诱导期和慢性期对动物进行了研究。HN的诱导与防御系统非特异性髓样成分的早期、显著但短暂的增加有关。随后，HN动物中B淋巴细胞谱系的细胞数量显著增加，这与整体体液免疫反应性的增加非常吻合。在这种实验性自身免疫疾病的发展过程中，未观察到T淋巴细胞亚群的改变。
