Abstract Rituximab (RTX) is a chimeric
monoclonal antibody (mAb) used for treatment of B cell lymphomas as well as for several autoimmune diseases. In vitro, RTX opsonization of CD20+ cells in the presence of serum promotes covalent deposition of large amounts of C3b(i) (C3 activation fragments) ultimately leading to cell lysis by the membrane attack complex. RTX-mediated C3b(i) deposition and cell killing are enhanced with the anti-C3b mAb 3E7; this enhancement does not occur with other anti-C3b(i) mAbs and killing is directed at B cells.
Fluorescence microscopy experiments suggest that C3b(i) is co-localized with bound RTX on B cells. However, <12% of deposited C3b(i) co-precipitates with