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International Immunology Advance Access published online on July 6, 2005
International Immunology, doi:10.1093/intimm/dxh287
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org
Received February 25, 2005
Accepted May 27, 2005

Article

Expression and function of TNF family member B cell-activating factor in the development of autoimmune arthritis

Min Zhang 1, King-Hung Ko 1, Queenie Lai Kwan Lam 1, Cherry Kam Chun Lo 1, Gopesh Srivastava 1, Bojian Zheng 2, Yu-Lung Lau 3, and Liwei Lu 1*

1 Department of Pathology, The University of Hong Kong, Pokfulam Road, Hong Kong, The People's Republic of China
2 Department of Microbiology, The University of Hong Kong, Pokfulam Road, Hong Kong, The People's Republic of China
3 Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pokfulam Road, Hong Kong, The People's Republic of China

* To whom correspondence should be addressed.
Liwei Lu, E-mail: liweilu{at}hkucc.hku.hk


  Abstract

B cell-activating factor (BAFF), a member of tumor necrosis factor family cytokines, has been shown to enhance the maturation and survival of peripheral B cells. While BAFF is implicated in regulating B cell function and autoimmunity, its role in the development of autoimmune arthritis has not been fully clarified. Using a collagen-induced arthritis (CIA) mouse model, we detected dysregulated expression of BAFF and its receptors in the peripheral lymphoid organs during arthritis induction. Elevated serum levels of BAFF were closely correlated with increased levels of anti-collagen antibodies during the CIA progression. Moreover, dendritic cells (DCs) and macrophages were found to express high amount of BAFF proteins at the acute and chronic stages of CIA, respectively. In cultures, recombinant BAFF suppressed apoptosis of splenic B cells from arthritic mice, and DC-induced B cell proliferation was specifically blocked by soluble decoy receptor B cell maturation antigen-Fc. These findings suggest that overproduction of BAFF by DCs and macrophages may play a crucial role in the pathogenesis of experimental arthritis.

Keywords: apoptosis; autoimmunity; B lymphocytes; cytokine; dendritic cells.
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