Immunoregulation in Heymann nephritis. I. Cell marker studies.

J Cornish, A Z Barabas, R Lannigan, J Rozing
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Abstract

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.

海曼肾炎的免疫调节。1 .细胞标记研究。
采用膜性肾小球肾病(MGN)模型海曼肾炎(Heymann nephroritis, HN)大鼠进行免疫调节实验。目前对HN中诱导和维持自身免疫反应的细胞免疫事件知之甚少。细胞标记研究利用荧光素(FITC)标记的单克隆抗体直接针对B细胞(Mark-I)和T细胞亚群:泛T (ER-I),辅助/诱导剂T (ER-2)和抑制/细胞毒性T (ER-3)。比较了正常和患病大鼠脾脏、淋巴结、外周血和骨髓的淋巴亚群。在疾病的诱导期和慢性期对动物进行研究。HN的诱导与防御系统的非特异性髓系成分的早期、显著但短暂的增加有关。随后,HN动物的B淋巴细胞系细胞数量显著增加,这与体液免疫反应性的总体增加相吻合。在这种实验性自身免疫性疾病的发展过程中,没有注意到T淋巴细胞亚群的改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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