Abstract
The production and oxidation mechanism of reactive oxygen species (ROS) are out of balance in rheumatoid arthritis (RA). However, the correlation between ROS and T cell subsets in RA remains unclear. Peripheral blood mononuclear cells (PBMCs) from patients with RA (n = 40) and healthy controls (n = 10) were isolated from whole blood samples. Synovial tissues (n = 3) and synovial fluid (n = 10) were obtained from patients with RA. The repartition of T cell subsets and expression of ROS and cytokines were examined according to RA severity. Fibroblast-like synoviocytes (FLSs) from patients with RA were stimulated with PBMCs and the expression of inflammation-related molecules were measured by RT-PCR and cytokine array. Regulatory T cells from patients with moderate (5.1 > DAS28 ≥ 3.2) RA showed the highest expression of mitochondrial ROS among the groups based on disease severity. Although ROS levels steadily increased with RA severity, there was a slight decline in severe RA (DAS28 ≥ 5.1) compared with moderate RA. The expression of inflammatory cytokines in RA FLSs were significantly inhibited when FLSs were co-cultured with PBMCs treated with ROS inhibitor. These findings provide a novel approach to suppress inflammatory response of FLSs through ROS regulation in PBMCs.
Highlights
Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation, synovial lining hyperplasia, and uncontrolled autoantibody production that results in cartilage damage and bone destruction [1]
We investigated whether RA severity is relevant to the characteristics of T cell subsets among Peripheral blood mononuclear cells (PBMCs)
Several studies have investigated whether abnormal repartition of T cell subsets is Several studies have investigated whether abnormal repartition of T cell subsets is associated with the pathogenic mechanisms of RA [23]
Summary
Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation, synovial lining hyperplasia, and uncontrolled autoantibody production that results in cartilage damage and bone destruction [1]. A large amount of type 1 helper T cells and IL-17–producing helper T cells (TH17s) infiltrate from peripheral blood into the synovium, where they secrete abundant pro-inflammatory cytokines/chemokines [3], induce the activation of fibroblast-like synoviocytes (FLSs) and synovial inflammation, and eventually contribute to disease severity [4]. In the early stages of RA, Tregs can downregulate the effector T cell response to help maintain joint homeostasis [10]. Treg expansion is often detected in inflamed joints, the suppressive function of Tregs is certainly impaired in RA, and T cell homeostasis is broken [11,12,13]
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