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Available online /content/6/5/197 Commentary The current status of targeting BAFF/BLyS for autoimmune diseases Meera Ramanujam and Anne Davidson Departments of Medicine and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA Corresponding author: Anne Davidson, davidson@ Received: 13 Apr 2004 Revisions requested: 6 Jul 2004 Revisions received: 7 Jul 2004 Accepted: 13 Jul 2004 Published: 29 Jul 2004 Arthritis Res Ther 2004, 6:197-202 (DOI 10.1186/ar1222) © 2004 BioMed Central Ltd Abstract It is increasingly recognized that B cells have multiple functions that contribute to the pathogenesis of autoimmunity. Specific targeting of B cells might therefore be an appropriate therapeutic intervention. The tumor necrosis factor-like molecule BAFF (BLyS) is a key B cell survival factor and its receptors are expressed on most peripheral B cells. Several different BAFF antagonists are under development and in early clinical trials. We review here the rationale for BAFF blockade, and its predicted mechanism of action in autoimmune diseases. Keywords: autoimmune diseases, B cells, BAFF (BLyS), co-stimulation, therapy Introduction like syndrome [10]. Thus, levels of BAFF must be tightly B cells are important in the pathogenesis of autoimmune regulated to maintain B cell survival without triggering disease. They produce autoantibodies that mediate tissue autoimmunity. injury, they function as antigen-presenting cells that present epitopes of self-antigen to autoreactive T cells, B cells express three different BAFF recep