Pathopysiological aspects of immune complex diseases. Part II. Phagocytosis, exocytosis, and pathogenic depositions

Abstract

Elimination of IC by the phagocytic system occurs mainly by macrophages and contrarotates to the pathogenic effect. Decisive to prevent systemic IC disease is the capacity of the phagocytic system. In the case of its saturation, the danger of the occurrence of IC disease is greatly enhanced. Conclusive evidence seems to exist that IC of extremely small or extremely high lattice structure (precipitates) are less pathogenic than soluble IC of medium network. Small IC in extreme antigen and antibody excess or precipitates exhibit a reduced complement activating potency. Small IC in extreme antigen or antibody excess hardly interact in vitro with membrane receptors and do not induce IC disease when injected or formed in vivo. Highly lattices IC, especially precipitates, are eliminated extremely quickly from the circulation, mainly by macrophages and there deposition in the kidney is significantly reduced. Thus, lack of quality of the antibody to precipitate the antigen and a reduced capacity and effectivity of the phagocytic system to eliminate the IC may be extremely important in the generation of IC diseases. Facing the overwhelming and partly even inconsistant data of this topic, one may doubt whether IC diseases may be regarded to be a defined and coherent disease. Too many variables and questions exist concerning the nature of the antigen, especially in tumor and autoimmune diseases, concerning the quality of the antibody and the characteristics of the pathogenic IC and concerning localization and the elimination process. Nevertheless, common pathophysiological pathways of IC diseases may be recognized.