The modulation of immune complex aggregation by classical pathway-mediated reactions.
Classical pathway (CP)-triggered reactions of complement-modulated immune complex (IC) aggregation (tetanus toxoid/human anti-tetanus toxoid-IgG; ICs of equivalence) were investigated turbidimetrically during the early stages of reaction. Monospecific Fab'- or Fab-fragments (rabbit) directed against certain complement components were used to block the complement function in normal human serum (NHS). Additionally, parts of the reactions were studied using purified complement components. C1q in serum generated by the addition of EDTA as well as purified C1q were found to increase the IC aggregation. In contrast to C1q, macromolecular C1 is able to inhibit IC aggregation, whereas additional participation of C-1 INH reversed this process. The cooperation of the remaining CP proteins (C4, C2, C4bp, and I) reconstituted the inhibition capacity of the complement. Whereas C3 supported significantly inhibition, a significant influence of other effector pathway (EP) components (C5-C9) was not detectable turbidimetrically.
D000936:Antigen-Antibody Complex / Q000276:immunology*; D003166:Complement Activating Enzymes / Q000276:immunology; D003167:Complement Activation; D003172:Complement C1 / Q000276:immunology; D003174:Complement C1 Inactivator Proteins / Q000276:immunology; D015922:Complement C1q; D003171:Complement Pathway, Classical; D003165:Complement System Proteins / Q000276:immunology*; D006801:Humans; D012995:Solubility
D000936:Antigen-Antibody Complex; D003172:Complement C1; D003174:Complement C1 Inactivator Proteins; D015922:Complement C1q; D003165:Complement System Proteins; D003166:Complement Activating Enzymes