Kelchner J, McIntosh J R, Boedecker E, Guggenheim S, McIntosh R M
Experientia. 1976 Sep 15;32(9):1204-8. doi: 10.1007/BF01927628.
Serial administration of mercuric chloride to rats was followed by development of antibodies to tubular basement membrane and renal tubular epithelial antigen (RTE) and glomerulonephritis characterized by granular deposits of hosts IgG, C3 and RTE along the glomerular capillary walls. The glomerular fixed antibody was directed against RTE. These studies suggest that tubular injury by mercury may lead to release of RTE and autosensitization and subsequent antibody production to this antigen result in formation of and glomerular deposition of circulating immunopathogenic complexes (RTE-anti-RTE) and glomerular morphologic alterations.
给大鼠连续注射氯化汞后，会产生针对肾小管基底膜和肾小管上皮抗原（RTE）的抗体，并引发肾小球肾炎，其特征是宿主IgG、C3和RTE沿肾小球毛细血管壁呈颗粒状沉积。肾小球固定抗体针对的是RTE。这些研究表明，汞引起的肾小管损伤可能导致RTE释放和自身致敏，随后针对该抗原产生抗体，导致循环免疫致病复合物（RTE-抗-RTE）形成并在肾小球沉积，进而引起肾小球形态改变。
