Data on arsenic trioxide modulates Treg/Th17/Th1/Th2 cells in treatment-naïve rheumatoid arthritis patients and collagen-induced arthritis model mice

In this article, we share the raw protein and mRNA data obtained from basal and stimulated human peripheral blood mononuclear cells (PBMCs) derived from 15 individual treatment-naïve rheumatoid arthritis (RA) patients and synovial fluid mononuclear cells (SFMCs). In treatment-naïve RA patients, PBMCs were treated with a gradient of concentrations of As(2)O(3) (0, 0.1, 0.5, 1.0, 2.0, 4.0 μM) for 48 hours. We found that 2.0 μM As(2)O(3) promoted the apoptosis of PBMCs significantly, and 0.5 μM As(2)O(3) was the lowest and effective concentration that contributed to Treg cell generation but it prevented Th17 cell differentiation, as assessed by flow cytometry. Furthermore, As(2)O(3) decreased the transcription factor STAT3 mRNA expression of Th17 cells but increased the transcription factor Foxp3 of Treg cells. In synovial fluid from RA patients, consistent with PBMCs, As(2)O(3) inhibited Th17 cell differentiation but promoted Treg cell generation. In an animal experiment, we analyzed the body-weight of mice as the indicator of As(2)O(3) toxicity and calculated the spleen index. As(2)O(3) significantly decreased the hematoxylin and eosin score in Type II collagen-induced arthritis in mice. Furthermore, As(2)O(3) downregulated the frequency of Th1 but upregulated Th2 cells. For more insight please see Arsenic trioxide improves Treg and Th17 balance by modulating STAT3 in treatment-naive rheumatoid arthritis patients [1].