Cell-mediated immunity in renal disease.

It has been shown in experimental models that cell-mediated immunologic mechanisms can lead to glomerular as well as tubulointerstitial renal injury, with or without concomitant antibody-mediated effects. The glomerular lesions are characterized by varying combinations of monocyte and, to a lesser extent, lymphocyte influx, necrosis, and proliferation of intrinsic glomerular cells. The tubulointerstitial lesions have generally been characterized by interstitial infiltrates containing numerous T lymphocytes and, often, numerous macrophages, sometimes with invasion of tubules and tubular cell damage. Although similar renal abnormalities are seen in several human renal diseases, further evidence is obviously required to establish a pathogenetic role for cellular immunity. Analyses of infiltrating mononuclear cells by immunohistochemical methods, with monoclonal antibodies that identify subsets of T cells, have indirectly supported a role for delayed hypersensitivity reactions in tubulointerstitial nephritis resulting from drugs or associated with anti-TBM antibodies, as well as a role for both delayed hypersensitivity and cytolytic lymphocyte effects in renal allografts. However, only with the development of methods that permit the identification of subsets of lymphocytes with unique functions, as well as the identification of the antigen specificity of the cells, will it be possible to understand fully the renal lesions that are now suspected of being cell-mediated.