Abstract
Mesenchymal stem cells (MSCs) are multi-potent cells that are self-renewable and possess the potential to differentiate into multiple lineages. Several studies demonstrated that MSCs could regulate a Th17/Treg balance and could be a potential therapeutic target for Rheumatoid Arthritis (RA). A20 is highly expressed in many cell types after the stimulation of TNF-α, where it may inhibit pro-inflammatory cytokine secretion. However, the expression of A20 in BM-MSCs in RA is not fully understood. In our study, we found that A20 was decreased in RA patients’ bone marrow MSCs (BM-MSCs), and with more IL-6 secretion, the balance of Th17/Treg was broken. In CIA mice, we found a moderate A20 decrease in mice MSCs as compared with those of control group in mRNA and protein levels. However, the IL-6 expression was increased. After umbilical cord MSCs treatment, A20 and IL-6 expressions were equal to the control group. Thus, our study indicates that loss of A20 in MSCs regulates the Th17/Treg balance in RA and the regulatory role of A20 in pro-inflammatory IL-6 production could be a potential target for the transfer of MSCs in RA adoptive therapy.
Highlights
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that has an incidence of 0.5% to 1%1, with high incidence in women and the elderly[2]
Expression of A20 was significantly decreased in Rheumatoid Arthritis (RA) (n = 11) BM-Mesenchymal stem cells (MSCs) samples compared with those of healthy controls (HCs)’ (n = 8)
Since human umbilical cord MSCs (UC-MSCs) that are easy to enrich share similarities with bone marrow MSCs (BM-MSCs) in immunogenicity and therapeutic function, UC-MSCs have been suggested as an alternative source of MSCs for cell therapy[22]
Summary
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that has an incidence of 0.5% to 1%1, with high incidence in women and the elderly[2]. Several clinical experiments have verified the therapeutic effect of MSCs. A non-randomized comparative clinical trial with RA patients who were unresponsive to classical medications[11], refers to that the function of MSCs treatment is correlate with increased numbers of Treg cells in peripheral blood, but the exact cause is misty. A non-randomized comparative clinical trial with RA patients who were unresponsive to classical medications[11], refers to that the function of MSCs treatment is correlate with increased numbers of Treg cells in peripheral blood, but the exact cause is misty These studies indicate MSCs have huge perspective in treating RA, but deep research is needed. A20, called TNF-α induced protein 3 (TNFAIP3), was firstly reported in 1990, which was induced by primary responsive gene stimulated by TNF-α in epithelial cell[12] We carry out this experiment to investigate the possible role of MSC A20 expression in RA development, and determine the underlying mechanism to seek for potential RA therapeutic target
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