Abstract
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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.