Supranutritional selenium suppresses ROS-induced generation of RANKL-expressing osteoclastogenic CD4+ T cells and ameliorates rheumatoid arthritis

超营养硒可抑制 ROS 诱导的 RANKL 表达破骨细胞 CD4+ T 细胞的生成并改善类风湿性关节炎

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作者:Jiahuan Qin, Xia Huang, Naiqi Wang, Pengcheng Zhou, Hao Zhang, Zhian Chen, Kaili Liang, Dongcheng Gong, Qunxiong Zeng, Peng Niu, Anping Chen, Lin Yuan, Zhaohui Yang, Linchong Su, Nan Shen, Jun Deng, Di Yu

Conclusion

Supranutritional Se suppresses RANKL-expressing osteoclastogenic CD4+ T cells and could be beneficial to RA, which warrants formal testing in randomised clinical trials.

Methods

Peripheral blood mononuclear cells (PBMCs) from RA patients (N = 57) and healthy controls (HC, N = 71) from an area of supranutritional Se intake (Enshi, Hubei, China) were analysed by flow cytometry. Serum cytokine and Se levels were measured by cytometric beads array (CBA) and inductively coupled plasma mass spectrometry (ICP-MS), respectively. With sufficient or supranutritional selenium intake, mice were induced with collagen-induced arthritis (CIA) and examined for disease activity and immunopathology. The influence of Se supplementation in the generation of RANKL-expressing osteoclastogenic CD4+ T cells was investigated by in vitro assays.

Objective

The benefit of Se supplementation in rheumatoid arthritis (RA) has been tested in clinical trials, but

Results

In Enshi city, HC showed the above-normal concentrations of serum Se concentrations while RA patients were enriched in the normal range (70-150 ng mL-1) or below. RA patients with higher Se levels demonstrated milder disease and lower levels of C-reactive protein, IL-6, RANKL and Th17 cells. In the mouse CIA model, supranutritional Se supplementation delayed disease onset, ameliorated joint pathology and reduced CD4+CD44+RANKL+ T cells. Se supplementation could suppress RANKL expression in cultured mouse Th17 cells.

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