The pathogenesis of glomerulonephritis in F1 hybrid mice injected with parental spleen cells was investigated in several ways. Whenever glomerulonephritis developed, the lesion had the typical morphology produced by antigen-antibody complexes. Experiments employing backcross mice demonstrated that the antigen is supplied by the recipient and that it is specified by the H-2 gene complex, or by a locus closely linked to H-2. The source of the antibody was investigated by staining glomerular lesions with fluorescein isothiocyanate-tagged anti-immunoglobulin allotype sera. Only donor-type allotypes could be detected. The ability of the donor's immunocytes to respond to the recipient's histocompatibility antigens in such a way as to produce nephritogenic immune complexes varied from strain to strain, and seemed to be controlled by a gene unrelated to H-2. The results suggest that cell surface antigens, such as histocompatibility antigens, may be of importance in the pathogenesis of several kinds of glomerulonephritis.
CHRONIC ALLOGENEIC DISEASE : III. GENETIC REQUIREMENTS FOR THE INDUCTION OF GLOMERULONEPHRITIS
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Helga Gleichmann, Ernst Gleichmann, Janine André-Schwartz, Robert S. Schwartz; CHRONIC ALLOGENEIC DISEASE : III. GENETIC REQUIREMENTS FOR THE INDUCTION OF GLOMERULONEPHRITIS . J Exp Med 1 March 1972; 135 (3): 516–532. doi: https://doi.org/10.1084/jem.135.3.516
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