The role of CD4+CD25+ T cells in autoantibody production in murine lupus

Authors

  • W.-T. Hsu,

    1. Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China,
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  • J.-L. Suen,

    1. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China, and
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  • B.-L. Chiang

    Corresponding author
    1. Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China,
    2. Department of Pediatrics, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China
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Bor-Luen Chiang MD, PhD, Department of Pediatrics, College of Medicine, National Taiwan University, No. 7, Chung-Shan South Road, Taipei, Taiwan, Republic of China.
E-mail: gicmbor@ha.mc.ntu.edu.tw

Summary

Systemic lupus erythematosus (SLE) is a chronic, systemic autoimmune disease characterized by the loss of tolerance to self-antigen. Because it is currently not known if regulatory T (Treg) cells are involved in the pathogenesis, we determined the frequency of CD4+CD25+ T cells and assayed the related gene expression levels in CD4+CD25+ T cells isolated from both lupus mice (NZB/NZW F1) and normal control mice (DBA2/NZW F1). The results showed that the frequency of CD4+CD25+ T cells in lupus mice was lower than that of normal mice. Except for the high expression level of interleukin (IL)-10 mRNA, CD4+CD25+ T cells from lupus mice expressed normal forkhead box P3 (Foxp3) and transforming growth factor (TGF)-β mRNA, and exerted suppressive functions. Furthermore, we depleted CD25+ Treg cells of non-autoimmune mice with anti-CD25 antibody and broke their tolerance with apoptotic cell-pulsed dendritic cells for the follow-up of autoantibody levels. The mice in the CD25+ cell-depleted group had higher titres of anti-double-strand/single-strand DNA antibodies than those of the isotype control antibody-treated group. These findings indicated that CD4+CD25+ T cells might be involved in the regulatory mechanism of autoantibody production.

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