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Experimental autoimmune glomerulonephritis in chickens. II. Adoptive transfer of disease with mononuclear cells
1Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville.
Autoimmune glomerulonephritis was induced in donor chickens by immunization with chicken, human, turkey or bovine glomeruli. Lymphocytes from the kidneys of each group and the spleen of donors immunized with chicken glomeruli were isolated and injected intravenously into six-week old syngeneic SC chickens. The disease was transferred to bursectomized/non-bursectomized recipients by cells from donors immunized with chicken and bovine glomeruli but not by cells from chickens immunized with human and turkey glomeruli. The transferred disease correlated with interstitial infiltrates in donors. No antibody was detected on the glomerular basement membrane or in the circulation of any recipients. Glomerulonephritis in this model can be transferred by specifically sensitized T lymphocytes alone without antibody. This new pathogenic process may play an important role in the development of glomerulonephritis in other animal models as well as in man, where minimal or no immune deposits are observed despite glomerulonephritis.
Autoimmune glomerulonephritis was induced in donor chickens by immunization with chicken, human, turkey or bovine glomeruli. Lymphocytes from the kidneys of each group and the spleen of donors immunized with chicken glomeruli were isolated and injected intravenously into six-week old syngeneic SC chickens. The disease was transferred to bursectomized/non-bursectomized recipients by cells from donors immunized with chicken and bovine glomeruli but not by cells from chickens immunized with human and turkey glomeruli. The transferred disease correlated with interstitial infiltrates in donors. No antibody was detected on the glomerular basement membrane or in the circulation of any recipients. Glomerulonephritis in this model can be transferred by specifically sensitized T lymphocytes alone without antibody. This new pathogenic process may play an important role in the development of glomerulonephritis in other animal models as well as in man, where minimal or no immune deposits are observed despite glomerulonephritis.