@article{oai:niigata-u.repo.nii.ac.jp:00016721, author = {河内, 裕}, issue = {5}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {May}, note = {Two nephritogenic monoclonal antibodies (mAbs) were produced in BALB/c mice immunized with rat glomeruli. The first mAb (mAb 5-1-6) identifies a 51-kDa protein (p51) on rat glomerular epithelial cell foot processes, mainly slit membrane and causes severe complement- and leukocyte-independent proteinuria when injected into rats. p51 first became detectable on the basal and lateral sides of the developing glomerular epithelium at the S-shaped body stage and became concentrated in the slit pore with the interdigitation of foot processes. p51 and ZO-1, a known component of tight junction, were closely localized at the slit membrane in the mature glomerulus but arrived at their final position from opposite directions. After mAb 5-1-6 injection, there was a progressive decline in stainnable ZO-1 and p51 in the glomerular epithelium of heavily proteinuric rats. We concluded that mAb 5-1-6 alters the molecular composition of the slit membrane and thereby affects the glomerular permeability barrier. The second mAb (mAb 1-22-3)binds the limited mesangial cell surface facing endothelial cells and causes the morphological changes similar to those induced by anti-thymocyte serum (ATS) and severe proteinuria in rats by a single i.v. injection. The mesangial lesion induced by ATS is reversible and not always accompanied with severe proteinuria. The model induced by the single injection of mAb 1-22-3 is also reversible. We succeeded in inducing irreversible mesangial changes with persistent proteinuria by two consecutive injections 2 weeks apart of a mAb 1-22-3. This model should be the best model to investigate the mechanism of chronic progression of human mesangial proliferative glomerulonephritis.}, pages = {219--225}, title = {単クローン抗体により惹起されるモデルを用いた糸球体腎炎の発症, 進行機序の解析}, volume = {112}, year = {1998} }