[Pathogenesis and therapy of glomerulonephritis. Reflections on recent advances]

The aim of this review is to describe how antibodies and cells of the immune system induce inflammatory lesions in the kidney. Renal glomeruli and tubules can be damaged not only by antibodies and immune complexes generated in the immune system but also by T lymphocyte-mediated hypersensitivity reactions originated locally. New mediators of inflammation have been identified, including growth factors and cytokines which are essential symbols of a language of intercellular communication modulating cell proliferation, the adhesion of inflammatory cells to the walls of the vessels, and to the extracellular matrix, and the formation of fibrosclerotic tissue contributing to the healing process. The identification of new methods for induction of tolerance to histocompatibility antigens, the identification of antigens responsible for autoimmune diseases of the kidney, and the synthesis of the peptides forming the receptor of T lymphocytes involved in the pathogenesis of an autoimmune disease of the brain, may help to design new therapeutic strategies for renal diseases, based on the inhibition of T lymphocyte activation.