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Rheumatology Advance Access originally published online on May 11, 2007
Rheumatology 2007 46(7):1083-1086; doi:10.1093/rheumatology/kem097
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Expression of B-cell activating factor of the tumour necrosis factor family (BAFF) in T cells in active systemic lupus erythematosus: the role of BAFF in T cell-dependent B cell pathogenic autoantibody production

S. Morimoto, S. Nakano, T. Watanabe, Y. Tamayama, A. Mitsuo, Y. Nakiri, J. Suzuki, K. Nozawa, H. Amano, Y. Tokano, T. Kobata1 and Y. Takasaki

Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo and 1Department of immunology, Dokkyo Medical University School of Medicine, Tochigi, Japan.

Correspondence to: S. Morimoto, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan. E-mail: morimoto{at}med.juntendo.ac.jp


  Abstract

Objectives. To determine whether B cell activating factor of the tumour necrosis factor family (BAFF) is involved in T cell-dependent B cell pathogenic autoantibody production in systemic lupus erythematosus (SLE).

Methods. Peripheral blood mononuclear cells (PBMCs) from 23 SLE patients were analysed by flow cytometry to examine the intracellular expression of BAFF in CD4+ and CD8+ T cells and the surface expression of BAFF-receptor (R) and TACI on CD20+ B cells. Moreover, peripheral blood was used to determine the level of BAFF messenger RNA (mRNA) in CD4+ and CD8+ T cells and the level of BAFF-R mRNA in CD20+ B cells. Blocking of BAFF function with TACI-Ig measured anti-double-stranded DNA (dsDNA) antibodies by enzyme-linked immunosorbent assay (ELISA).

Results. CD4+ and CD8+ T cells from patients with active SLE expressed intracellular BAFF whereas those from normal subjects did not. BAFF-R and TACI were expressed on B cells from both normal controls and patients with active SLE and there was no significant difference. CD4+ and CD8+ T cells from SLE patients expressed BAFF mRNA whereas those from normal controls did not. Expression of BAFF-R mRNA in CD20+ B cells showed no significant difference between SLE patients and normal controls. TACI-Ig suppressed spontaneous in vitro T cell-dependent B cell anti-dsDNA antibodies production on active SLE with kidney involvement.

Conclusions. BAFF may play a pathogenic role in SLE by stimulating T cell-dependent B cell autoantibodies production. Blockade of BAFF is a promising therapeutic approach for SLE especially in patients with kidney involvement.

KEY WORDS: Systemic lupus erythematosus, BAFF, T cell, Autoantibody production

Submitted 19 October 2006; revised version accepted 21 March 2007.
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