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Death receptor 3 signaling enhances proliferation of human regulatory T cells
Author(s) -
Bittner Sebastian,
Knoll Gertrud,
Ehrenschwender Martin
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12632
Subject(s) - immune system , receptor , mapk/erk pathway , signal transduction , immunology , microbiology and biotechnology , stimulation , biology , cancer research , neuroscience , genetics
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 ( DR 3), a member of the TNF ‐receptor superfamily ( TNFRSF ), increases Treg frequency and efficiently controls exuberant immune activation. For human Tregs, neither DR 3 expression nor potential functions have been described. Here, we show that human Tregs express DR 3 and demonstrate DR 3‐mediated activation of p38, ERK , and NF κB. DR 3 stimulation enhances Treg expansion ex vivo while retaining their suppressive capacity. In summary, our results establish a functional role for DR 3 signaling in human Tregs and could potentially help to tailor Treg‐based therapies.