HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Melchers, F Search for Related Content PubMed PubMed Citation Articles by Melchers, F

Actions of BAFF in B cell maturation and its effects on the development of autoimmune disease

Biozentrum, Department of Cell Biology, University of Basel, Basel, Switzerland

Correspondence to:
Correspondence to:
Dr F Melchers, Biozentrum, Department of Cell Biology, University of Basel, Klingelbergstrasse 50–70, CH-4056 Basel, Switzerland;
fritz.melchers{at}unibas.ch

ABSTRACT
BAFF, a member of the family of tumour necrosis factor (TNF) ligands, is essential for the development of peripheral mature, long lived B lymphocytes. It binds to three different receptors, BCMA, TACI, and BAFF-R, which are all members of the family of TNF receptors. Defects in the genes encoding BAFF or BAFF-R abolish the generation of mature B cells. BAFF is made by myeloid cells whereas BAFF-R is expressed preferentially on B cells. BAFF induces polyclonal maturation of resting, short lived immature B cells to resting, long lived mature B cells without proliferation. Lupus erythematodes prone mice have elevated blood levels of BAFF, and treatment of these mice with the BAFF decoy receptor (BCMA-Ig) prevents the onset of this systemic autoimmune disease. Human lupus patients also have elevated blood levels of BAFF. Treatment with BAFF neutralising agents (decoy receptors, monoclonal antibodies) should prevent, delay, or, at least, slow down the disease.

Keywords: BAFF; B cell maturation; autoimmune disease

This article has been cited by other articles:

				P. Neri, S. Kumar, M. T. Fulciniti, S. Vallet, S. Chhetri, S. Mukherjee, Y. Tai, D. Chauhan, P. Tassone, S. Venuta, et al. Neutralizing B-Cell Activating Factor Antibody Improves Survival and Inhibits Osteoclastogenesis in a Severe Combined Immunodeficient Human Multiple Myeloma Model Clin. Cancer Res., October 1, 2007; 13(19): 5903 - 5909. [Abstract] [Full Text] [PDF]

				G. CARLIZZI, M. V. CIARLA, A. DI LUZIO, R. LABRIOLA, D. FRATTOLILLO, P. SPIRIDIGLIOZZI, C. MASALA, and R. STROM Autoantibodies in Patients with Monoclonal Gammopathies Ann. N.Y. Acad. Sci., June 1, 2007; 1107(1): 206 - 211. [Abstract] [Full Text] [PDF]

				M P Cancro The BLyS/BAFF family of ligands and receptors: key targets in the therapy and understanding of autoimmunity Ann Rheum Dis, November 1, 2006; 65(suppl_3): iii34 - iii36. [Abstract] [Full Text] [PDF]

				M. Zhang, K.-H. Ko, Q. L. K. Lam, C. K. C. Lo, G. Srivastava, B. Zheng, Y.-L. Lau, and L. Lu Expression and function of TNF family member B cell-activating factor in the development of autoimmune arthritis Int. Immunol., August 1, 2005; 17(8): 1081 - 1092. [Abstract] [Full Text] [PDF]

				O. Cohavy, J. Zhou, C. F. Ware, and S. R. Targan LIGHT Is Constitutively Expressed on T and NK Cells in the Human Gut and Can Be Induced by CD2-Mediated Signaling J. Immunol., January 15, 2005; 174(2): 646 - 653. [Abstract] [Full Text] [PDF]

				Y. Sasaki, S. Casola, J. L. Kutok, K. Rajewsky, and M. Schmidt-Supprian TNF Family Member B Cell-Activating Factor (BAFF) Receptor-Dependent and -Independent Roles for BAFF in B Cell Physiology J. Immunol., August 15, 2004; 173(4): 2245 - 2252. [Abstract] [Full Text] [PDF]

				O. Cohavy, J. Zhou, S. W. Granger, C. F. Ware, and S. R. Targan LIGHT Expression by Mucosal T Cells May Regulate IFN-{gamma} Expression in the Intestine J. Immunol., July 1, 2004; 173(1): 251 - 258. [Abstract] [Full Text] [PDF]