Rehabilitation or the death penalty: Autoimmune B cells in the dock

Abstract

CD20‐based monoclonal antibodies have become established as treatments for lymphoma, rheumatoid arthritis, systemic lupus erythematosus, vasculitis and dermatomyositis, with the principle therapeutic mechanism relating to B‐cell depletion through effector cell engagement. An article by Brühl et al. in this issue of the European Journal of Immunology [Eur. J. Immunol. 2015. 45: 705–715] reveals a fundamentally distinct mechanism of silencing autoimmune B‐cell responses. Rather than B‐cell depletion, the authors use anti‐CD79b antibodies to induce B‐cell tolerance and suppress humoral immune responses against collagen to prevent the development of arthritis in mice. Here we highlight the differences in the mechanisms used by anti‐CD20 and anti‐CD79b Ab therapy and discuss why depletion of B cells may not be required to treat autoimmune arthritis and other B‐cell‐associated pathologies.