[Contribution of experimental pathology to the understanding of human immune glomerulonephritis]

Immune glomerulonephritis (GN) progresses in three phases. Induction corresponding to the development of immune response; transduction characterized by the appearance of immunological reactants in the glomerulus, and mediation responsible for glomerular lesions and proteinuria. Studies of experimental models have resulted in significant advances in our understanding of these phases. The most striking acquisitions concern the genetic control of GN and its link with the major histocompatibility system; the identification of target antigens involved in Goodpasture's syndrome and in experimental epimembranous GN; the re-evaluation of the role played by circulating immune complexes in the in situ formation of immune complexes in the glomerular capillary wall; the identification of numerous mediatory systems (notably cytokines) which play an important part in glomerular inflammation and in the development of fibrosis. These advances may lead, in the short- or medium-term, to interesting therapeutic novelties.