Abstract
Studies were undertaken to elucidate the characteristics of IgA immune complexes responsible for glomerular deposition and complement activation. Monomeric IgA antidinitrophenyl (DNP) and the antigen DNP-Ficoll tended to form small soluble complexes that circulated in the blood without localizing in glomeruli of experimental animals. In contrast, polymeric IgA formed intermediate and large-sized complexes that caused glomerular immune deposits. Although covalently cross-linked large-sized IgA oligomers deposited in the glomeruli, they failed to induce concomitant deposition of complement components. Only the presence of a complement-activating antigen endowed the glomerular IgA immune deposits with the ability to activate complement. Thus, the size of the IgA complexes plays a primary role in initiating glomerular localization, and the nature of the antigen causes a secondary phase of inflammation.
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