Autoreactive B cells play a role in autoimmune diseases via their production of circulating autoantibodies and/or their role as antigen-presenting cells for autoreactive T cells after the capture of self antigens by cell surface autoantibodies that increase their antigen-presentation capabilities (i). Rituximab and other anti-CD20 mAbs cross-link CD20 on the surface of B cells and induce B cell depletion mainly through ADCC, although complement-dependent cytotoxicity (CDC) and apoptosis have also been implicated (ii). Anti-CD20–mediated B cell depletion prevents interaction with autoreactive T cells (iii) and reduces the amount of circulating autoantibodies (iv), although with much slower kinetics. Finally, as suggested by Hu et al. in their study in this issue of the