The role of immune complexes formed in situ has been most extensively studied in the Heymann nephritis model in the rat, a human counterpart of membranous nephropathy (MN). This is a non-proliferative form of GN in which the humoral, Th2 responses play an important role. In human idiopathic MN, an increase in the percentage of IL-4 (Masutani et al. 2004) and IL-10 (Hirayama et al. 2002) was observed in peripheral blood T cells, which correlated with the amount of proteinuria. Following induction of the disease, antibodies against gp330, megalin (Cavallo 1994; Ronco and Debiec 2005), are deposited at the subepithelial space of the glomerulus and trigger podocyte injury.
