Abstract
Autoimmune diseases are due to a breakdown of the tolerant state to autologous constituents. Some autoimmune diseases, including kidney diseases, can occur spontaneously in man. Our present understanding of the pathogenesis of human autoimmune diseases, however, is based mainly on the results of studies of diseases induced in laboratory animals by appropriate immunization. These diseases usually involve strong immunization such as incorporation of autologous tissue in “adjuvants,” like Freund's adjuvant, or immunization of animals with a similar tissue from a different species that shares cross-reactive antigens. Autoimmune reactions can be manifested by the production of autoantibodies and/or of autoreactive T cells. Thus, tissue damage may result from the reaction of antibodies with antigens present in the kidney, from tissue deposition of circulating immune complexes, and from cellular immune processes (1, 2). These mechanisms of hypersensitivity are not mutually exclusive. It is only for didactic reasons that we arbitrarily classify the various autoimmune renal diseases as if they were induced by a single pathogenic mechanism (Table I). In this review two groups of animal models of nephritis will be described. In the first group kidney lesions are induced by autoantibodies reacting with structural kidney antigens such as those of basement membranes or those present on the surface of cells. In immunofluorescence microscopy the immune reactants may be found along basement membranes in either a linear (e.g., in antibasement membrane nephritis) or a granular pattern (e.g., in Heymann glomerulonephritis). In the second group the nephropathies are conceivably the result of deposition in the kidney of circulating autologous immune complexes. The immune complexes accumulate in a granular pattern. Where possible, we will present evidence that similar diseases occur in man. Because insufficient solid data are available, a separate discussion of the role of autoreactive T cells in the development of kidney diseases is not included in this review.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have