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Immunologically mediated lesions of kidney tubules and interstitium in laboratory animals and in man

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Conclusion

In recent years, animal models of TI nephritis attributable to humoral immune mechanisms have become firmly established. Results of immunopathology studies indicate that similar mechanisms might be involved in a small fraction of human TI nephritides. In some patients the contribution of humoral immune mechanisms to TI lesions may not have been recognized in tissue specimens obtained at late stages of disease.

In laboratory animals as well as in man insufficient information is available to appraise the possible significance of immediate-type hypersensitivity and cell-mediated immune reactions in the induction and perpetuation of TI lesions. More studies on these two immune effector mechanisms are needed to clarify the pathogenesis of TI nephritis that, in the majority of the patients, is still not understood.

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Authors and Affiliations

  1. Departments of Pathology, Microbiology, and Medicine, State University of New York at Buffalo, USA

    Jan R. Brentjens, Bernice Noble & Giuseppe A. Andres

  2. Kidney Research Laboratory of the Buffalo General Hospital, Buffalo, New York, USA

    Jan R. Brentjens, Bernice Noble & Giuseppe A. Andres

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  1. Jan R. Brentjens
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  2. Bernice Noble
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  3. Giuseppe A. Andres
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This work has been supported by Grants AI 10334 and AM 26394 of the National Institutes of Health, U.S. Public Health Service

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Brentjens, J.R., Noble, B. & Andres, G.A. Immunologically mediated lesions of kidney tubules and interstitium in laboratory animals and in man. Springer Semin Immunopathol 5, 357–378 (1982). https://doi.org/10.1007/BF01892093

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