Experimental studies on factors causing acute serum sickness glomerulonephritis of immune complex origin. I. The role of immune complexes and the immunological status of the host.
In acute serum sickness glomerulonephritis induced in rabbits by large doses of BSA, the relationship of the host's immunological status and the severity of renal histological changes was studied. It was found that good antibody producers developed more severe renal lesions. The higher avidity of antibodies enhances the inflammatory effect of immune complexes. Kidney is favoured for deposition of immune complexes especially in the case of chronic immune complex formation in the presence of antigen excess. Diminished phagocytic function of leukocytes (probably decreased immune complex saturating capacity) may also contribute to the severity of renal histological alterations.
D000208:Acute Disease; D000818:Animals; D000917:Antibody Formation; D000936:Antigen-Antibody Complex; D005921:Glomerulonephritis / Q000276:immunology*; D007109:Immunity; D007668:Kidney / Q000276:immunology / Q000473:pathology; D011817:Rabbits; D012710:Serum Albumin, Bovine / Q000009:adverse effects; D012713:Serum Sickness / Q000276:immunology*; D014018:Tissue Distribution
D000936:Antigen-Antibody Complex; D012710:Serum Albumin, Bovine