Abstract
Abstract Tetrandrine (TET) is a purified chemical compound with well-established anti-inflammatory and immunosuppressive properties. The underlying mechanism of its immunosuppressive effect remains incompletely understood. It is also reported that membrane-bound (mTNF) is more effective than soluble TNF to expand Tregs through TNFR2. Therefore, we examined the effect of TET on TNF expression on dendritic cells (DCs) and its effect on Tregs in wildtype and TNFR2 KO mice. We found that, TET didn’t directly expand Tregs in vitro. But TET increased mTNF expression on DC2.4 cells and human monocyte-derived DCs. In addition, these effects of TET weren’t due to LPS contamination. Intraperitoneal injection of TET into wildtype mice increased the number of Tregs by ~1.5-fold compared with control mice. TNFR2 expression was up-regulated on Tregs rather than Teffs by TET treatment. However, the number of Tregs wasn’t changed by TET in TNFR2 KO mice. Taken together, our study revealed that TET promoted mTNF expression on DCs and consequently expanded Tregs via mTNF-TNFR2 signaling. Therefore, this represents a novel mechanism underlying the anti-inflammatory effect of TET.
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