title: 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.
authors: Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, General Hospital, University of Southampton, Southampton, UK.
authors: Lekh N
authors: LN
authors: Dahal
authors: Mark S
authors: MS
authors: Cragg
mesh_terms: D000818:Animals; D000906:Antibodies / Q000627:therapeutic use*; D001168:Arthritis / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology* / Q000473:pathology; D051925:CD79 Antigens / Q000037:antagonists & inhibitors* / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects*; D008212:Lymphocyte Depletion / Q000379:methods; D051379:Mice
chemical_list: D000906:Antibodies; D051925:CD79 Antigens; C497883:CD79B protein, human
keywords: Anti-CD20; Antibody therapy; Arthritis; B-cell tolerance; CD79b