Evans B D, Dilwith R L, Balaban S L, Rudofsky U H
Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany.
Int Arch Allergy Appl Immunol. 1988;86(2):238-42. doi: 10.1159/000234578.
Mice immunized with rabbit renal basement membranes form autoantibodies to their kidney glomerular and tubular basement membranes (GBM/TBM). Development of renal tubular disease (RTD) consists of deposition of autoantibodies along the GBM/TBM with the inter- and intratubular accumulation of lymphocytes and macrophages and destruction of the TBM. Transfer of this disease in mice with either serum or monoclonal antibodies, however, has been difficult to demonstrate and, therefore, attempts were made to confirm a report that RTD is passively transferred by anti-TBM autoantibodies. Using the revised protocol in this later report, we found that 12 weeks after transfer autoantibodies were deposited along the GBM and/or TBM of the recipients, yet RTD was not observed. Although qualitative and quantitative characteristics of the antibody may play a role in the pathogenesis in the murine model of RTD, we could not obtain evidence to support and confirm this study.
用兔肾基底膜免疫的小鼠会形成针对其肾小球和肾小管基底膜(GBM/TBM)的自身抗体。肾小管疾病(RTD)的发展包括自身抗体沿GBM/TBM沉积,伴有淋巴细胞和巨噬细胞在肾小管间和管内积聚以及TBM破坏。然而,用血清或单克隆抗体在小鼠中传递这种疾病一直难以证实,因此,有人试图证实一份关于RTD可由抗TBM自身抗体被动传递的报告。使用该后续报告中的修订方案,我们发现转移12周后,自身抗体沿受体的GBM和/或TBM沉积,但未观察到RTD。尽管抗体的定性和定量特征可能在RTD小鼠模型的发病机制中起作用,但我们无法获得支持和证实该研究的证据。