Experimental autoimmune glomerulonephritis in chickens.
A definite role of the humoral immune system in experimental autoimmune glomerulonephritis (EAG) has been shown. However, the role of the cellular immune system is less clear. Difficulty in separating these two systems has previously precluded examination of their isolated roles in the pathogenesis of EAG. The development of a chicken model of EAG would obviate these difficulties. We immunized chickens with bovine glomerular basement membrane (GBM) in complete Freund's adjuvant. The resultant disease is associated with circulating antibody to both chicken and bovine GBM and in vivo deposition of chicken IgG along the GBM in a linear pattern with minimal fixation of chicken complement. The lesion consists of proliferative glomerulonephritis as indicated by an increase in glomerular size and a decrease in the ratio of tuft size to the number of nuclei present. The proliferative component involves mainly the mesangium with little alteration of the capillary loops. In addition to proliferation of the glomerular tuft, there are associated adhesions and small crescents. No abnormal proteinuria developed in test animals compared to controls through 22 weeks of observation, although animals did develop proteinuria after intravenous colloidal carbon. Renal function remained normal throughout the period of our observations. The present study demonstrates that EAG can be successfully produced in chickens. This model affords the opportunity to examine the isolated roles of the humoral and cellular immune systems in the pathogenesis of EAG.
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D001485:Basement Membrane / Q000276:immunology; D002645:Chickens / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D005921:Glomerulonephritis / Q000276:immunology* / Q000473:pathology; D007678:Kidney Glomerulus / Q000276:immunology; D011507:Proteinuria / Q000276:immunology