Studies on the pathogenic roles of antigens isolated from renal tubular cells in the classical Heymann nephritis

Abstract

In order to analyze the antigens (Ags) which cause Heymann nephritis (HN) and mechanisms of IC formation in the subepithelial site of GBM, we isolated two Ags from renal tubular epithelium (RTE) from Wistar rats and prepared rabbit antiserum against these Ags. Classical HN was induced by immunization with crude renal tissue suspension by the method of Heymann et al. Immunofluorescence method in normal rat kidney revealed that the Ag with MW of 65 KD (= beta) existed not only in RTE, but also in the glomerular capillary wall. On the other hand, the Ag with MW of 35 KD (= gamma) only existed in RTE. Circulating Abs and glomerular eluted Abs from the kidney of classical HN, reacted to RTE only by indirect immunofluorescence. Soluble Fx1A, beta and gamma were electrophoresed on SDS-PAGE gels and transblotted onto nitrocellulose membrane, anti beta Abs reacted to several bands including 330 KD band of Fx1A and beta Ag. However anti gamma Abs reacted to only 330 KD band of Fx1A and gamma Ags. On the other hand, Glomerular eluted Abs from the kidney of classical HN reacted to several bands of Fx1A and gamma Ag, but not to beta Ag. These facts suggest that beta and gamma are components of 330 KD protein of Fx1A. The gamma Ag is thought to be one of the major pathogenic Ag in HN.