ARTICLE

Helga Gleichmann ¹, Ernst Gleichmann ¹, Janine André-Schwartz ¹, and Robert S. Schwartz ¹

¹ From the Clinical Immunology Service, New England Medical Center Hospitals, and the Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111

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.

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