Jäckle B, Schubothe H
Immun Infekt. 1980;8(2):50-5.
In the last ninety years there were many attempts to induce immune haemolytic anaemia (IHA) in laboratory animals. The techniques employed were injections of modified autologous or incompatible erythrocytes as well as hyperimmunization with material of high antigen activity (e.g. egg albumin). Serious temporary IHA could be induced occasionally. The main pathogenetic mechanism in this immune reaction was related to the antigen. Another model used was the so called graft-host-reaction in which IHA is based on antibody formation of transplanted immunocompetent cells towards the host erythrocytes. So far, the best animal model is the spontaneous autoimmune haemolytic anaemia in NZB-mice. However this model has not been completely evaluated. In these animals AIHA is mediated by a genetically prescribed immunoregulatory defect which may be located at the level of T-lymphocytes.
在过去的九十年里，人们多次尝试在实验动物中诱发免疫性溶血性贫血（IHA）。采用的技术包括注射经修饰的自体或不相容红细胞，以及用高抗原活性物质（如卵白蛋白）进行超免疫。偶尔可以诱发严重的暂时性IHA。这种免疫反应的主要发病机制与抗原有关。另一种使用的模型是所谓的移植物抗宿主反应，其中IHA基于移植的免疫活性细胞对宿主红细胞的抗体形成。到目前为止，最佳的动物模型是NZB小鼠的自发性自身免疫性溶血性贫血。然而，这个模型尚未得到全面评估。在这些动物中，自身免疫性溶血性贫血是由遗传规定的免疫调节缺陷介导的，该缺陷可能位于T淋巴细胞水平。
