The complement subcomponent Clq mediates binding of immune complexes and aggregates to endothelial cells in vitro*
The present studies were initiated to investigate whether soluble immune complexes, upon interaction with complement, can bind to endothelial cells. Human umbilical vein endothelial cells (HUVE) were incubated with purified human lz5I-1abeled Clq at 4°C in RPMI-0.5% bovine serum albumin and assayed for binding. Optimal binding of '251-labeled Clq to HUVE was reached within 2 h, and saturation of binding was found at concentrations of 5 pg/well input. The binding of '251-labeled Clq was inhibitable with unlabeled Clq and by the collagenous region of pepsin-cleaved Clq. 30 inhibition was observed with the globular heads of Clq, suggesting that Clq binds to HUVE via the collagenous region of Clq. When HUVE were first reacted with various concentrations of Clq, washed and subsequently incubated with 1251-labeled aggregated human IgM (AIgM), binding of lz51-1abeled AIgM to HUVE occurred depending on the dose of Clq. Only those aggregates of IgM which react with Clq in a solid-phase C l q binding assay were able to bind to HUVE presensitized with Clq. In addition it was shown that C l q mediated binding of aggregated IgG to HUVE. Furthermore, immune complexes (IC), that were prepared with bovine thyroglobulin (BTg) and rabbit anti-BTg, bound to Clqpreincubated HUVE. These studies suggest that localization of IC on endothelium can be enhanced following interaction of the IC with complement.