Immune complexes disease transfer

Whereas complement and its role in immune complex diseases have been described above (Sect. D.1.2), there appears to be a number of instances of untoward reactions to drugs in which complement activation may play a major role. Anaphylactic reactions have been described following the development of drug-specific antibodies of the IgG type capable of activating complement. In some cases, such as an immediate-type reaction following the intravenous injection of protamine sulfate (Lakin et al. 1978), homocy to tropic antibodies of IgG type capable of passively transferring the reaction have been demonstrated. Such antibodies have a short sensitization period, are stable to heating at 56 °C and seem to require complement to induce the anaphylactic reaction. 

Major histocompatibility complex (MHC) Class 11 molecules are believed to bind to a 3 (IV) NCI epitopes stimulating T-cell recognition and modulating the humoral response. Using a mouse model of GBM disease, Kalluri and colleagues (30) showed that all mice strains immunized with a3 (IV) NCI peptides developed anti a3 (IV) NCI antibodies but the development of pulmonary and renal disease was restricted to Swiss James Lambert (SJL) mice that possessed MHC H-2 . B6 (H-2 ), BALB/c (H-2 ), DBA/2 (H-2 ) mice developed only renal disease and A/J (H-2 ), AKR (H-2 ), and CBA (H-2 ) mice showed no evidence of either renal or pulmonary disease. In addition, these investigators showed that passive transfer of isogenic a3 (IV) NCI antibodies into T-cell receptor-deficient mice did not cause renal or pulmonary injury. Further immunohistochemical studies supported a Thl response pattern with increased presence of interleukin (IL)-12, lL-4, IL-10, and... 

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