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Open Access Highly Accessed Research article

Increased interleukin-23 receptor+ T cells in peripheral blood mononuclear cells of patients with systemic lupus erythematosus

Hathaipat Puwipirom1, Nattiya Hirankarn123*, Pimpayao Sodsai1, Yingyos Avihingsanon14, Jongkonnee Wongpiyabovorn123 and Tanapat Palaga25*

Author Affiliations

1 Lupus Research Unit, Chulalongkorn University, Phayathai Road, Pathumwan, Bangkok 10330, Thailand

2 Medical Microbiology Interdisciplinary Program, Graduate School, Chulalongkorn University, Phayathai Road, Pathumwan, Bangkok 10330, Thailand

3 Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Phayathai Road, Pathumwan, Bangkok 10330, Thailand

4 Department of Medicine, Faculty of Medicine, Chulalongkorn University, Phayathai Road, Pathumwan, Bangkok 10330, Thailand

5 Department of Microbiology, Faculty of Science, Chulalongkorn University, Phayathai Road, Pathumwan, Bangkok 10330, Thailand

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Arthritis Research & Therapy 2010, 12:R215  doi:10.1186/ar3194

Published: 29 November 2010

Abstract

Introduction

Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by production of autoantibodies and immune complex deposition in various organs. Aberrations in the T lymphocyte compartment and dysregulated cytokine production are key features of SLE pathogenesis and disease progression. Recently, the role of the interleukin (IL)-17/IL-23 axis in the pathogenesis of SLE has been reported. IL-23 and IL-23R are essential for expansion of pathogenic IL-17-producing T lymphocytes and have been shown to be important in the pathogenesis of lupus in animal models.

Methods

In this study, the expression of IL-23R and IL-17 in CD4+ and CD8+ T lymphocytes in peripheral blood mononuclear cells (PBMCs) of SLE patients and control subjects were examined by flow cytometry. Twenty-nine SLE patients and 10 control subjects were recruited in this study. Patients were divided into active and inactive groups based on the SLE disease activity index (SLEDAI). As another disease control population, five psoriatic patients were recruited in this study.

Results

Percentages of both IL23R+ CD4+ and IL-23R+ CD8+ T cell subsets were significantly higher in freshly isolated PBMCs from both groups of SLE patients compared to control subjects (P = 0.0021 and P = 0.0006, respectively). In addition, this difference was maintained after ex vivo stimulation with plate-bound anti-CD3/CD28 antibodies (P = 0.007 and P = 0.0019, respectively). When the fold increase in IL-17+ T cells after ex vivo stimulation for three days was compared between patients and controls, SLE patients exhibited significantly higher increases in CD4+ IL-17+ and CD8+ IL-17+ T cells, suggesting that PBMCs from SLE patients promoted the expansion of IL-17-producing T cells upon stimulation more vigorously than control PBMCs. These trends were not observed in psoriasis patients. The correlations between IL-23R+ T cells and IL-17+ T cells and IL-23R+ CD8+ T cells and SLEDAI scores in patients were also found to be statistically significant.

Conclusions

The results of our study confirmed the relevance of the IL-23/IL-17 axis in the pathogenesis of SLE and further highlighted the importance of IL-23R+ T cell subsets in this autoimmune disease.