Acute immune complex disease in rabbits. The role of complement and of a leukocyte-dependent release of vasoactive amines from platelets.
By depletion of C3 from rabbits undergoing acute experimental immune complex disease with an anticomplementary factor in cobra venom, it has been possible to demonstrate that deposition of the complexes in arteries and glomeruli does not require the complement components reacting after C2. Immunological reactions, in which platelets release their vasoactive amines, have been examined in rabbits undergoing immune complex disease. A correlation was obtained between the presence of a complement-independent reaction which required blood leukocytes, antigen and platelets, the deposition of immune complexes, and the induction of glomerulonephritis. C3 depletion did, however, have a marked alleviating effect on the severity of the arterial lesions. Neutrophil accumulation and the subsequent necrotizing arteritis were prevented. In contrast, the character and severity of the glomerulonephritis was not altered by depletion of later-acting complement components.
D000818:Animals; D001792:Blood Platelets / Q000378:metabolism*; D002499:Centrifugation, Density Gradient; D003165:Complement System Proteins / Q000032:analysis / Q000502:physiology*; D005921:Glomerulonephritis / Q000473:pathology; D006636:Histamine Release; D005779:Immunodiffusion; D007962:Leukocytes / Q000276:immunology; D011507:Proteinuria; D011817:Rabbits; D012711:Serum Albumin, Radio-Iodinated / Q000032:analysis; D012713:Serum Sickness / Q000276:immunology*; D012911:Snakes; D014688:Venoms
D012711:Serum Albumin, Radio-Iodinated; D014688:Venoms; D003165:Complement System Proteins