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Experimental data suggest that the B-cell antigen CD20 may play a significant role in the pathogenesis of many diseases including glomerular diseases. These and other findings underpin the central concept of B-cell-depleting therapies that target CD20 antigen as treatments for lupus nephritis, idiopathic membranous nephropathy, focal segmental glomerulosclerosis, cryglobulinemic glomerulonephritis, antibody mediated renal allograft rejection and recurrent glomerulonephritis in renal allograft. Use of rituximab as a B-cell depleting therapy has been associated with clinical improvement and has emerged as a possible adjunct or alternative treatment option in this field of nephrology.
Rituximab mode of action: apoptosis and ADCC. Rituximab mediated apoptosis is thought to…
Figure 1
Rituximab mode of action: apoptosis and ADCC. Rituximab mediated apoptosis is thought to be a consequence of caspase-3 activation. Complement activation by the Fc portion of the antibody leading to cell lysis is another mode of action of rituximab. Rituximab also induces ADCC mediated by a variety of effector cells (natural killer cells, granulocytes and macrophages). ADCC in the presence of rituximab represent killing of B cells by effector cells that are activated by binding to the Fc portion of the chimeric anti-CD20 molecule.
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