The clearance of circulating IgA immune complexes following acute bile duct obstruction was investigated in this study. IgA immune complexes were formed in uitro from MOPC-315, an IgA M-component with anti-dinitrophenyl (DNP) specificity, and '251-DNPlo bovine serum albumin (BSA). Eighteen hours after laparotomy during "which the common bile duct was either identified only or identified and ligated, the IgA immune complexes were injected intravenously. Groups of bile duct-ligated and bile duct-patent rats were also injected intravenously with IgG anti-DNP-'2SI-DNPloBSA immune complexes and '261-bovine liver j3-glucuronidase to assess the hepatic clearance of materials not dependent on a n intact biliary system. Clearance of IgA immune complexes was delayed after bile duct ligation. Although the clearance of IgA immune complexes was delayed, only 10% of these complexes remained in the circulation at 3 hr. The clearance of IgG immune complexes and j3-glucuronidase was not affected by ligation. These experiments demonstrate the physiologic importance of a patent bile duct in the normal clearance of IgA immune complexes in the rat. The observation that clearance is delayed, but not completely inhibited by bile duct ligation suggests that alternate mechanisms exist for removing IgA immune complexes from the circulation.
Recent experiments demonstrated that immune complexes can form in the circulation of rats injected with IgA antibody and the corresponding antigen (1,2). These complexes appear to be removed from the circulation, at least in part, by transport into bile in the rat or mouse (2-6). In these species, transfer into bile of IgA immune complexes proceeded by a secretory component (SC)dependent mechanism (3), was blocked by excess free IgA but not by IgG or IgM (7), and did not involve galactose-or mannose-specific glycoprotein receptors of the liver (7). To further assess the importance of the hepatobiliary clearance of antigen-antibody complexes