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Rheumatology Advance Access originally published online on December 26, 2007
Rheumatology 2008 47(2):145-149; doi:10.1093/rheumatology/kem327
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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

Role of pathogenic auto-antibody production by Toll-like receptor 9 of B cells in active systemic lupus erythematosus

S. Nakano, S. Morimoto, J. Suzuki, K. Nozawa, H. Amano, Y. Tokano and Y. Takasaki

Department of Rheumatology and Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.

Correspondence to: S. Nakano, Department of Rheumatology and Internal Medicine, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-Ku, Tokyo 113-8421, Japan. E-mail: soubey{at}med.juntendo.ac.jp


  Abstract

Objectives. Toll-like receptor 9 (TLR9) is a pattern-associated receptor functioning in innate immunity that may be involved in the recognition of self-antigens and the production of pathogenic auto-antibodies. Therefore, we examined the expression of TLR9 in systemic lupus erythematosus (SLE) to determine whether TLR9 is involved in the production of pathogenic auto-antibodies.

Methods. B cells were collected from patients with active SLE, and subjected to analysis of the TLR9 molecule using flow cytometry fluorescence activated cell sorting (FACS) and TLR9 mRNA by reverse-transcriptase polymerase chain reaction. SLE B cells were stimulated with CpG-ODN, and subsequent cytokine and anti-dsDNA antibody production was measured by enzyme-linked immunosorbent assay.

Results. The expression and mRNA level of TLR9 on B cells was up-regulated in SLE patients, and SLE disease activity index (SLEDAI) and CH50 were correlated with TLR9 expression on CD20+ B cells. Moreover, TLR9–CpG interaction enhanced the production of anti-dsDNA antibody and IL-10.

Conclusions. The present study demonstrated that higher expression of TLR9 on peripheral blood B cells from patients with active SLE was significantly correlated with CH50 and SLEDAI to TLR9, and induced the production of anti-dsDNA antibody and IL-10 by TLR9–CpG ligation. These results suggest that an abnormality of innate immunity plays a crucial role in the pathology of SLE, and that blockade of CpG–TLR9 interaction may be a new therapeutic approach for SLE.

KEY WORDS: SLE, B cells, Toll-like receptor 9, CpG-DNA, Anti-dsDNA antibody, IL-10, SLEDAI, CH50, Innate immunity

Submitted 21 May 2007; revised version accepted 2 November 2007.
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