title: Chronic allogeneic disease. 3. Genetic requirements for the induction of glomerulonephritis.
abstract: The pathogenesis of glomerulonephritis in F(1) 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.
mesh_terms: D000818:Animals; D000936:Antigen-Antibody Complex; D000941:Antigens; D002908:Chronic Disease; D005921:Glomerulonephritis / Q000209:etiology / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D006648:Histocompatibility; D006824:Hybridization, Genetic; D007154:Immune System Diseases / Q000235:genetics* / Q000473:pathology; D005779:Immunodiffusion; D007125:Immunogenetics; D007678:Kidney Glomerulus / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D008854:Microscopy, Electron; D008856:Microscopy, Fluorescence; D013154:Spleen / Q000166:cytology / Q000276:immunology
chemical_list: D000936:Antigen-Antibody Complex; D000941:Antigens