Autoregulation of autoantibody synthesis in mercuric chloride nephritis in the Brown Norway rat II. Presence of antigen‐augmentable plaque‐forming cells in the spleen is associated with humoral factors behaving as auto‐anti‐idiotypic antibodies
Autoregulation of autoantibody synthesis in mercuric chloride nephritis in the Brown Norway rat II. Presence of antigen‐augmentable plaque‐forming cells in the spleen is associated with humoral factors behaving as auto‐anti‐idiotypic antibodies
复制标题
挪威布朗大鼠 II 型氯化汞肾炎中自身抗体合成的自身调节脾脏中抗原可增强斑块形成细胞的存在与表现为自身抗独特型抗体的体液因子有关。
DOI：
10.1002/eji.1830140516
复制
发表时间：
1984
影响因子：
5.4
通讯作者：
C. Lockwood
中科院分区：
文献类型：
--
作者：
J. Chalopin;C. Lockwood
使用斑块形成细胞（PFC）测定法在体外研究了给予HgCl 2的挪威布朗（BN）大鼠的自限性抗肾小球基底膜（GBM）自身抗体反应中的免疫调节机制。峰值脾PFC反应发生在第9天，此后反应急剧下降，很少检测到后12天。在特异性研究中，第9天在动物PFC试验中掺入可溶性GBM有两种不同的影响。在一些动物中，PFC反应以剂量依赖性方式受到抑制;然而，在其他动物中观察到PFC数量增加。此外，在第12天（或之后）研究的某些动物的PFC混合物中加入GBM，发现了大量GBM特异性PFC，而在标准PFC试验中最初未观察到GBM特异性PFC。将来自这些动物的血清（含和不含抗原增强型PFC）掺入含有从第9天动物采集的细胞的PFC混合物中。来自显示斑块的动物的血清可以抑制第9天动物的GBM特异性PFC反应，而来自没有显示斑块的动物的血清不能。因此，来自自身抗体水平下降的BN大鼠的血清可以在自身免疫应答的早期阶段抑制动物细胞的GBM特异性空斑形成能力，并显示了体液因子、嘌呤类抗独特型抗体在该模型中影响自身抗体形成的自身调节中的潜在重要性。
Plaque‐forming cell (PFC) assays were used to investigate in vitro the immunoregulatory mechanism operating in the self‐limiting anti‐glomerular basement membrane (GBM) autoantibody response of Brown Norway (BN) rats given HgCl2. The peak splenic PFC response occurred at day 9; thereafter the response fell sharply and was rarely detected after day 12. In specificity studies, incorporation of soluble GBM in the PFC assays of animals at day 9 had two distinct effects. In some animals the PFC response was inhibited in a dose‐dependent fashion; however, in others an augmented number of PFC was observed. Furthermore, addition of GBM to the PFC mixture from certain animals studied at day 12 (or after) revealed large numbers of GBM‐specific PFC when originally no GBM‐specific PFC had been observed in the standard PFC assay. Sera from such animals, with and without antigen‐augmentable PFC, were incorporated in the PFC mixture containing cells taken from day 9 animals. Sera from animals with revealed plaques could inhibit the GBM‐specific PFC response of day 9 animals, whereas sera from animals without revealed plaques could not. Thus sera, from BN rats whose own antibody levels were falling, could inhibit the GBM‐specific plaque‐forming capability of cells from animals at an earlier stage of the autoimmune response and showed the potential importance of humoral factors, putatively anti‐idiotypic antibodies, in effecting autoregulation of autoantibody formation in this model.