期刊
PLOS ONE
卷 11, 期 8, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0161507
关键词
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资金
- German Research Foundation [SFB650, TP28, GRK1121, TPB1, LO1542/3-1]
- German Federal Ministry of Education and Research (e:Bio/T-Sys) [0316164G]
- Swiss National Science Foundation (Sinergia) [CRSII3 160772/1]
- Volkswagen Foundation (Lichtenberg Program)
- Willy Robert Pitzer Foundation (Osteoarthritis Research Program)
- International Max Planck Research School for Infectious Diseases and Immunology
- European Molecular Biology Organization (EMBO) long-term fellowship [ALTF 116-2012, ALTF 314-2012]
- [330621]
- Swiss National Science Foundation (SNF) [CRSII3_160772] Funding Source: Swiss National Science Foundation (SNF)
Immunomodulatory Foxp3(+) regulatory T cells (Tregs) form a heterogeneous population consisting of subsets with different activation states, migratory properties and suppressive functions. Recently, expression of the IL-33 receptor ST2 was shown on Tregs in inflammatory settings. Here we report that ST2 expression identifies highly activated Tregs in mice even under homeostatic conditions. ST2(+) Tregs preferentially accumulate at non-lymphoid sites, likely mediated by their high expression of several chemokine receptors facilitating tissue homing. ST2(+) Tregs exhibit a Th2-biased character, expressing GATA-3 and producing the Th2 cytokines IL-5 and IL-13 -especially in response to IL-33. Yet, IL-33 is dispensable for the generation and maintenance of these cells in vivo. Furthermore, ST2(+) Tregs are superior to ST2(-) Tregs in suppressing CD4(+) T cell proliferation in vitro independent of IL-33. This higher suppressive capacity is partially mediated by enhanced production and activation of the anti-inflammatory cytokines IL-10 and TGF beta. Thus, ST2 expression identifies a highly activated, strongly suppressive Treg subset preferentially located in non-lymphoid tissues. Here ST2(+) Tregs may be well positioned to immediately react to IL-33 alarm signals. Their specific properties may render ST2(+) Tregs useful targets for immunomodulatory therapies.
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