Formation of soluble immune complexes by complement in sera of patients with various hypocomplementemic states. Difference between inhibition of immune precipitation and solubilization.
To examine whether the ability of complement to form soluble immune complexes plays a role in preventing immune complex-mediated diseases, we analyzed the capacity of complement to inhibit immune precipitation (IIP) and to solubilize preformed immune aggregates (SOL) in 23 sera of patients with various hypocomplementemic states, and we correlated the results of these studies with the clinical syndromes found in the various patients. In sera with deficiency or depletion of early classical pathway components, IIP was profoundly altered, whereas SOL was delayed but in the normal range. In contrast, in sera with C3 depletion but intact classical pathway and in properdin-deficient serum, IIP was initially preserved, whereas SOL was abolished. Since the incidence of immune complex diseases in various hypocomplementemic states correlates with the severity of IIP defects, but not with reduced SOL, it is suggested that IIP is an essential biological function of complement that prevents the rapid formation of insoluble immune complexes in vivo.
D000936:Antigen-Antibody Complex; D011232:Chemical Precipitation; D003176:Complement C3 / Q000172:deficiency; D015938:Complement Membrane Attack Complex; D003171:Complement Pathway, Classical; D003165:Complement System Proteins / Q000172:deficiency*; D006801:Humans; D007105:Immune Complex Diseases / Q000276:immunology*; D011414:Properdin / Q000172:deficiency; D012995:Solubility
D000936:Antigen-Antibody Complex; D003176:Complement C3; D015938:Complement Membrane Attack Complex; D011414:Properdin; D003165:Complement System Proteins