期刊
FEBS LETTERS
卷 591, 期 8, 页码 1187-1195出版社
WILEY
DOI: 10.1002/1873-3468.12632
关键词
DR3; TL1A; TNFRSF25; TNFSF15; Treg
资金
- Deutsche Forschungsgemeinschaft (DFG) [EH465/2-1]
- Universitatsstiftung Angela Schotz-Keilholz
- Medical Faculty of the University of Regensburg (ReForM-B program)
Exploiting regulatory T cells (Tregs) to control aberrant immune reactions is a promising therapeutic approach, but is hampered by their relative paucity. In mice, activation of death receptor 3 (DR3), a member of the TNF-receptor superfamily (TNFRSF), increases Treg frequency and efficiently controls exuberant immune activation. For human Tregs, neither DR3 expression nor potential functions have been described. Here, we show that human Tregs express DR3 and demonstrate DR3-mediated activation of p38, ERK, and NFjB. DR3 stimulation enhances Treg expansion ex vivo while retaining their suppressive capacity. In summary, our results establish a functional role for DR3 signaling in human Tregs and could potentially help to tailor Treg-based therapies.
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