Robert M. Lewis D.V.M.¹, Martine Y. K. Armstrong M.D.¹, Janine André-Schwartz M.D.¹, Asuman Muftuoglu M.D.¹, Lorraine Beldotti ¹, and Robert S. Schwartz M.D.¹

¹ From the Clinical Immunology Service, New England Medical Center Hospitals, the Department of Medicine, Tufts University School of Medicine, Boston 02111, and the Department of Bacteriology and Immunology, Harvard Medical School, Boston, Massachusetts 02115

Glomerulonephritis, often accompanied by the nephrotic syndrome, developed in CAF₁ mice following the administration of spleen cells from normal BALB/c mice. The renal lesion was membranous glomerulonephritis. When studied with fluorescein-conjugated antisera to either mouse gamma globulin or ß_1C-globulin, the glomeruli contained beaded and irregular deposits of these immunoproteins. The ultrastructure of the lesion was characterized by thickening of the glomerular basement membranes and the presence of electron-dense subepithelial deposits. Acid eluates of the diseased kidneys contained gamma globulin that failed to bind to sections of normal kidneys. These findings conform to the type of nephritis provoked by immune complexes. They indicate that this type of immune injury can be based on the reaction of intolerant immunocytes to normal antigens.

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