WEKO3
アイテム
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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
http://hdl.handle.net/10191/45831
http://hdl.handle.net/10191/458315dc13b19-1d02-4911-b980-303d197e30d8
名前 / ファイル | ライセンス | アクション |
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112(5)_219-225.pdf (1.3 MB)
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Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2017-01-30 | |||||
タイトル | ||||||
タイトル | 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 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | 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 | |||||
言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | monoclonal antibody | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | proteinuria | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | slit membrane | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | glomerular epithelial cell | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | mesangial cell | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | 単クローン抗体 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | 蛋白尿 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | スリット膜 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | 糸球体上皮細胞 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | メサンギウム細胞 | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | departmental bulletin paper | |||||
その他のタイトル | ||||||
その他のタイトル | Pathogenesis of the Experimental Models of Glomerulonephritis Induced by Monoclonal Antibodies | |||||
著者 |
河内, 裕
× 河内, 裕 |
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著者別名 | ||||||
識別子 | 106111 | |||||
識別子Scheme | WEKO | |||||
姓名 | Kawachi, Hiroshi | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 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. | |||||
書誌情報 |
新潟医学会雑誌 en : 新潟医学会雑誌 巻 112, 号 5, p. 219-225, 発行日 1998-05 |
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出版者 | ||||||
出版者 | 新潟医学会 | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00290440 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN00182415 | |||||
著者版フラグ | ||||||
値 | publisher |