Experimental analysis on organ allergy of hapten-bound renal tubular basement membrane

将三硝基苯酚缀合的卵清蛋白高度阳离子化（等电点>10），并进行凝胶过滤以获得单体（42 kDa）。将抗原选择性地注射到Wistar大鼠的左肾动脉中。通过免疫组织化学在冷冻切片上记录抗原定位;它以线性模式沉积在肾小管基底膜（TBM）和Bowman囊上，但不在肾小球基底膜上，并且在抗原注射后保持长达36 h。在对照组中，非阳离子化的单体TNP-OA（42 kDa，等电点=4.6）仅在肾小管上皮细胞中显示细颗粒沉积，而在TBM上不显示。在阳离子抗原注射后24 h，用抗TNP-human IgG兔血清转移诱导肾小管间质性肾炎（TIN）伴嗜酸性浸润。用苦酰氯皮肤致敏7天后，对具有TNP特异性细胞免疫的大鼠注射阳离子抗原，诱发急性肾小管坏死。该病变与人类过敏性肾炎的病变不同，可能是由于TNP毒性所致。在预先注射阳离子抗原的未致敏C57/BL 6小鼠中，针对TNP的脾T细胞（CD 4+或CD 8+）的转移不有助于TIN诱导。

Trinitrophenol-conjugated ovalbumin was highly cationized (isoelectric point>10) and was subjected to gel filtration to obtain monomer (42 kDa). The antigen was injected selectively into the left renal arteries of Wistar rats. Antigen localization was documented by immunohistochemistry on frozen section ; it was deposited in a liner pattern on the tubular basement membrane (TBM) and Bowman's capsule but not on the glomerular basement membrane, and remained up to 36 h after the antigen injection. In control, non-cationized, monomeric TNP-OA (42 kDa, isoelectric point=4.6) showed fine granular deposition in the tubular epithelium exclusivery, but not on the TBM.Tubulointerstitial nephritis (TIN) with neutrophilic infiltration was induced by the serum transfer of antiTNP-human IgG rabbit serum 24 h after cationic antigen injection. Acute tubular necrosis was induced after cationic antigen injection in the rats which were 7 days-previously skin-sensitized by picryl chloride to have TNP-specific cellular immunity. The lesion was not similar to the lesion of human hypersensitivity nephritis and may due to the TNP-toxicity. The transfer of splenic T cell (either CD4+ or CD8+) against TNP did not contribute to TIN-induction in the non-sensitized C57/BL6 mice which were previously injected with the cationic antigen.