Abstract
BackgroundSystemic lupus erythematosus (SLE) is an autoimmune disease characterized by T-cell-dependent B-cell activation and altered T-cell response. Co-stimulatory and co-inhibitory molecules regulate and exert T-cell differentiation, survival and cytokine production. CD134+ and PD-1+ T-cells in SLE patients are increased in SLE. The aim of this study was to characterize CD134+ and PD-1+CD4+ T-cells according to their ability to produce IFN-γ, IL-21 and IL-22 in SLE patients.MethodsPeripheral blood of 39 SLE patients and 19 healthy controls (HC) was stimulated with phorbol myristate acetate (PMA) calcium ionophore (Ca-Io). The expression of IFN-γ, IL-21 and IL-22 T-cells within the CD134+ and PD-1+ T-cells was analyzed by flow cytometry. Disease activity was assessed by SLE Disease Activity Index.ResultsPeripheral unstimulated CD134+ and PD-1+ CD4+ T-cells were significantly increased in patients with lupus nephritis. Upon stimulation both, CD134+ and PD-1+ CD4+ T-cells, produced significantly less IFN-γ in SLE patients as compared to HC. The percentages of IL-22 within the CD134+CD4+ T-cells were also significantly decreased in SLE as compared to HC.ConclusionCD134+ and PD-1+CD4+ T-cells have mainly a Th1 effector T-cell signature. A lower proportion produces also IL-21 and IL-22. The impaired capacity to produce IFN-γ and IL-22 in SLE patients may contribute to the pathogenesis of the disease.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by T-cell-dependent B-cell activation and altered T-cell response
The percentages of CD134+CD4+ T-cells were significantly increased in SLE patients as compared to healthy controls (21.4 ± 10.4% vs. 13.7 ± 5.8%; p = 0.002)
The percentages of CD134+CD4+ T-cells were significantly increased in active SLE patients as compared to healthy controls (24.8 ± 12.2% vs. 13.7 ± 5.8%; p = 0.02) and between inactive SLE patients versus healthy controls
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by T-cell-dependent B-cell activation and altered T-cell response. Co-stimulatory and co-inhibitory molecules regulate and exert T-cell differentiation, survival and cytokine production. Beside the activation of B-cells via co-stimulatory molecules, T-cells exert effector functions by the production of proinflammatory cytokines. Effector functions, including cytokine production, expansion and survival, are enhanced by co-stimulatory molecules such as CD134 (OX40) [4, 5]. We demonstrated an increased expression of the co-stimulatory molecule CD134 (OX40) on T-cells in systemic lupus erythematosus (SLE) patients especially with lupus nephritis [6]. Co-inhibitory receptors such as PD-1 were increased in C D4+CD25neg T-cells of SLE patients [7] Both the co-stimulatory molecule CD134 and co-inhibitory molecule PD-1 are expressed
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