Nephrotoxic Serum Nephritis in Complement Intact and Deficient Mice

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Abstract
In 1962, Rosenberg and Tachibana reported that certain strains of mice lacked hemolytic complement (C′) activity (1). The lack of C′ is genetically controlled (2) and related to the absence of a β migrating globulin (3, 4). The C′ deficient mice are able to make an immune response to this globulin, which they lack but which is present in C′ intact strains (3, 4). Nilsson and Müller-Eberhard have identified the deficient globulin as analogous to human β1F-globulin (5) which in the human C′ sequence is C′5. The C′ deficient mice lack C′5 activity (6) while having normal C′1,4 and 2 activities (7) and β1c-globulin (C′3) (8, 9). C′ deficient mice have normal phagocytosis of bacteria (10), are able to reject allogeneic skin grafts (11) and develop Arthus reactions (8, 12). They may develop passive cutaneous anaphylaxis with rabbit antibody but only when large amounts are employed (13).