001     140709
005     20240321220848.0
024 7 _ |a 10.1016/j.immuni.2019.03.014
|2 doi
024 7 _ |a pmid:31027998
|2 pmid
024 7 _ |a 1074-7613
|2 ISSN
024 7 _ |a 1097-4180
|2 ISSN
024 7 _ |a altmetric:59402713
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037 _ _ |a DZNE-2020-07031
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Schmidleithner, Lisa
|0 P:(DE-2719)2812337
|b 0
|e First author
|u dzne
245 _ _ |a Enzymatic Activity of HPGD in Treg Cells Suppresses Tconv Cells to Maintain Adipose Tissue Homeostasis and Prevent Metabolic Dysfunction.
260 _ _ |a New York, NY
|c 2019
|b Elsevier
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2019-05-01
336 7 _ |a article
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|s 1709893056_26558
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Regulatory T cells (Treg cells) are important for preventing autoimmunity and maintaining tissue homeostasis, but whether Treg cells can adopt tissue- or immune-context-specific suppressive mechanisms is unclear. Here, we found that the enzyme hydroxyprostaglandin dehydrogenase (HPGD), which catabolizes prostaglandin E2 (PGE2) into the metabolite 15-keto PGE2, was highly expressed in Treg cells, particularly those in visceral adipose tissue (VAT). Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ)-induced HPGD expression in VAT Treg cells, and consequential Treg-cell-mediated generation of 15-keto PGE2 suppressed conventional T cell activation and proliferation. Conditional deletion of Hpgd in mouse Treg cells resulted in the accumulation of functionally impaired Treg cells specifically in VAT, causing local inflammation and systemic insulin resistance. Consistent with this mechanism, humans with type 2 diabetes showed decreased HPGD expression in Treg cells. These data indicate that HPGD-mediated suppression is a tissue- and context-dependent suppressive mechanism used by Treg cells to maintain adipose tissue homeostasis.
536 _ _ |a 341 - Molecular Signaling (POF3-341)
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542 _ _ |i 2019-05-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
542 _ _ |i 2020-05-21
|2 Crossref
|u http://www.elsevier.com/open-access/userlicense/1.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a STAT5 Transcription Factor
|2 NLM Chemicals
650 _ 7 |a 15-ketoprostaglandin E2
|0 2S0F1FTK13
|2 NLM Chemicals
650 _ 7 |a Hydroxyprostaglandin Dehydrogenases
|0 EC 1.1.1.-
|2 NLM Chemicals
650 _ 7 |a Dinoprostone
|0 K7Q1JQR04M
|2 NLM Chemicals
650 _ 2 |a 3T3 Cells
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Cell Line
|2 MeSH
650 _ 2 |a Diabetes Mellitus, Type 2: metabolism
|2 MeSH
650 _ 2 |a Dinoprostone: analogs & derivatives
|2 MeSH
650 _ 2 |a Dinoprostone: metabolism
|2 MeSH
650 _ 2 |a HEK293 Cells
|2 MeSH
650 _ 2 |a Homeostasis: immunology
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Hydroxyprostaglandin Dehydrogenases: genetics
|2 MeSH
650 _ 2 |a Hydroxyprostaglandin Dehydrogenases: metabolism
|2 MeSH
650 _ 2 |a Insulin Resistance: genetics
|2 MeSH
650 _ 2 |a Intra-Abdominal Fat: cytology
|2 MeSH
650 _ 2 |a Intra-Abdominal Fat: immunology
|2 MeSH
650 _ 2 |a Jurkat Cells
|2 MeSH
650 _ 2 |a Lymphocyte Activation: immunology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a STAT5 Transcription Factor: metabolism
|2 MeSH
650 _ 2 |a T-Lymphocytes, Regulatory: enzymology
|2 MeSH
650 _ 2 |a T-Lymphocytes, Regulatory: immunology
|2 MeSH
700 1 _ |a Thabet, Yasser
|b 1
700 1 _ |a Schönfeld, Eva
|b 2
700 1 _ |a Köhne, Maren
|0 P:(DE-2719)2812698
|b 3
|u dzne
700 1 _ |a Sommer, Daniel
|b 4
700 1 _ |a Abdullah, Zeinab
|b 5
700 1 _ |a Sadlon, Timothy
|b 6
700 1 _ |a Osei-Sarpong, Collins
|0 P:(DE-2719)2813660
|b 7
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700 1 _ |a Subbaramaiah, Kotha
|b 8
700 1 _ |a Copperi, Francesca
|b 9
700 1 _ |a Haendler, Kristian
|b 10
700 1 _ |a Varga, Tamas
|0 P:(DE-2719)2812488
|b 11
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700 1 _ |a Schanz, Oliver
|b 12
700 1 _ |a Bourry, Svenja
|0 P:(DE-2719)2811740
|b 13
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700 1 _ |a Bassler, Kevin
|b 14
700 1 _ |a Krebs, Wolfgang
|b 15
700 1 _ |a Peters, Annika E
|b 16
700 1 _ |a Baumgart, Ann-Kathrin
|b 17
700 1 _ |a Schneeweiss, Maria
|b 18
700 1 _ |a Klee, Kathrin
|b 19
700 1 _ |a Schmidt, Susanne V
|b 20
700 1 _ |a Nüssing, Simone
|b 21
700 1 _ |a Sander, Jil
|b 22
700 1 _ |a Ohkura, Naganari
|b 23
700 1 _ |a Waha, Andreas
|b 24
700 1 _ |a Sparwasser, Tim
|b 25
700 1 _ |a Wunderlich, F Thomas
|b 26
700 1 _ |a Förster, Irmgard
|b 27
700 1 _ |a Ulas, Thomas
|0 P:(DE-2719)9000845
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700 1 _ |a Weighardt, Heike
|b 29
700 1 _ |a Sakaguchi, Shimon
|b 30
700 1 _ |a Pfeifer, Alexander
|b 31
700 1 _ |a Blüher, Matthias
|b 32
700 1 _ |a Dannenberg, Andrew J
|b 33
700 1 _ |a Ferreirós, Nerea
|b 34
700 1 _ |a Muglia, Louis J
|b 35
700 1 _ |a Wickenhauser, Claudia
|b 36
700 1 _ |a Barry, Simon C
|b 37
700 1 _ |a Schultze, Joachim L
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700 1 _ |a Beyer, Marc
|0 P:(DE-2719)2812219
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773 1 8 |a 10.1016/j.immuni.2019.03.014
|b : Elsevier BV, 2019-05-01
|n 5
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|t Immunity
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|y 2019
|x 1074-7613
773 _ _ |a 10.1016/j.immuni.2019.03.014
|g Vol. 50, no. 5, p. 1232 - 1248.e14
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Marc 21