Abstract
Myeloid-derived suppressor cells (MDSCs) comprise of a population of cells, which suppress the innate and adaptive immune system via different mechanisms. MDSCs are accumulated under pathological conditions. The present study aimed to clarify the pathological role of MDSCs in systemic lupus erythematosus (SLE) patients. Consequently, the level of circulating M-MDSCs was significantly increased in newly diagnosed SLE patients as compared to healthy controls. An elevated level of M-MDSCs was positively correlated with the disease severity in SLE patients and an immunosuppressive role was exerted in an iNOS-dependent manner. The decrease in the number of M-MDSCs after therapy rendered them as an indicator for the efficacy of treatment. These results demonstrated that M-MDSCs participated in the pathological progress in SLE patients. Thus, MDSCs are attractive biomarkers and therapeutic targets for SLE patients.
Highlights
Systemic lupus erythematosus (SLE) is one of the most common autoimmune diseases [1]
We investigated the frequency of M-Myeloid-derived suppressor cells (MDSCs) in 32 newly diagnosed SLE patients, as well as 30 age- and sex-matched healthy controls
In CD14+ monocytes and Peripheral blood mononuclear cells (PBMCs), the frequency of monocytic MDSCs (M-MDSCs) was significantly higher in SLE patients than that in healthy controls (Figures 1A–C)
Summary
Systemic lupus erythematosus (SLE) is one of the most common autoimmune diseases [1]. The main manifestations include the imbalance of peripheral immune tolerance to autoantigens. The excessive activation of T cells and the production of a large number of autoantibodies due to the hyperfunction of B cells disrupt the steady state of pro-inflammatory and anti-inflammatory factors as well as the accumulation of large amounts of immune complexes and inflammatory damage to multiple organs and tissue systems [2]. The equilibrium in the immune system and its strict control by regulatory mechanisms is a critical issue in SLE. Several individual cell subsets or molecules are involved in the pathogenesis of SLE. The specific pathogenesis is not yet clearly understood
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