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Clinical and Developmental Immunology
Volume 2013, Article ID 405395, 9 pages
Research Article

Elevated Apoptosis and Impaired Proliferation Contribute to Downregulated Peripheral γδ T Cells in Patients with Systemic Lupus Erythematosus

1Department of Rheumatology and Immunology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China
2Department of Rheumatology and Immunology, The Affiliated Hospital of Nantong University, Nantong 226000, China
3Department of Rheumatology and Immunology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China

Received 8 May 2013; Accepted 17 July 2013

Academic Editor: Guixiu Shi

Copyright © 2013 Zhimin Lu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. To investigate the frequency of peripheral γδ T cells in patients with systemic lupus erythematosus (SLE) and its correlation with disease activity and to analyze the apoptotic status, proliferation ability, and intracellular cytokine profile of these cells. Methods. Flow cytometry was performed to detect the percentage and intracellular cytokine expression of peripheral γδ T cells from SLE patients. Annexin-V/PI double staining was applied to determine the proportion of apoptotic γδ and CD3+ T cells. γδ T cell proliferation was analyzed by CFSE labeling technique. Results. The percentage and absolute number of γδ T cells were remarkably decreased in active SLE patients compared to those in inactive patients and healthy controls, with γδ T cell count negatively correlated with disease activity. Compared with healthy controls, peripheral γδ T cells from active SLE patients exhibited higher apoptotic rate and lower proliferation ability, as well as elevated expression of intracellular IFN-γ, IL-4, IL-10, and TGF-β, but not IL-17 or Foxp3. Conclusion. Decreased γδ T cells in the peripheral blood of SLE patients might be caused by upregulated apoptosis and downregulated cell proliferation. These γδ T cells may secret both pro- and anti-inflammatory cytokines to perform their functions in SLE.