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000140709 0247_ $$2doi$$a10.1016/j.immuni.2019.03.014
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000140709 0247_ $$2ISSN$$a1097-4180
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000140709 037__ $$aDZNE-2020-07031
000140709 041__ $$aEnglish
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000140709 1001_ $$0P:(DE-2719)2812337$$aSchmidleithner, Lisa$$b0$$eFirst author$$udzne
000140709 245__ $$aEnzymatic Activity of HPGD in Treg Cells Suppresses Tconv Cells to Maintain Adipose Tissue Homeostasis and Prevent Metabolic Dysfunction.
000140709 260__ $$aNew York, NY$$bElsevier$$c2019
000140709 264_1 $$2Crossref$$3print$$bElsevier BV$$c2019-05-01
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000140709 520__ $$aRegulatory 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.
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000140709 542__ $$2Crossref$$i2019-05-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000140709 542__ $$2Crossref$$i2020-05-21$$uhttp://www.elsevier.com/open-access/userlicense/1.0/
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000140709 650_7 $$2NLM Chemicals$$aSTAT5 Transcription Factor
000140709 650_7 $$02S0F1FTK13$$2NLM Chemicals$$a15-ketoprostaglandin E2
000140709 650_7 $$0EC 1.1.1.-$$2NLM Chemicals$$aHydroxyprostaglandin Dehydrogenases
000140709 650_7 $$0K7Q1JQR04M$$2NLM Chemicals$$aDinoprostone
000140709 650_2 $$2MeSH$$a3T3 Cells
000140709 650_2 $$2MeSH$$aAnimals
000140709 650_2 $$2MeSH$$aCell Line
000140709 650_2 $$2MeSH$$aDiabetes Mellitus, Type 2: metabolism
000140709 650_2 $$2MeSH$$aDinoprostone: analogs & derivatives
000140709 650_2 $$2MeSH$$aDinoprostone: metabolism
000140709 650_2 $$2MeSH$$aHEK293 Cells
000140709 650_2 $$2MeSH$$aHomeostasis: immunology
000140709 650_2 $$2MeSH$$aHumans
000140709 650_2 $$2MeSH$$aHydroxyprostaglandin Dehydrogenases: genetics
000140709 650_2 $$2MeSH$$aHydroxyprostaglandin Dehydrogenases: metabolism
000140709 650_2 $$2MeSH$$aInsulin Resistance: genetics
000140709 650_2 $$2MeSH$$aIntra-Abdominal Fat: cytology
000140709 650_2 $$2MeSH$$aIntra-Abdominal Fat: immunology
000140709 650_2 $$2MeSH$$aJurkat Cells
000140709 650_2 $$2MeSH$$aLymphocyte Activation: immunology
000140709 650_2 $$2MeSH$$aMale
000140709 650_2 $$2MeSH$$aMice
000140709 650_2 $$2MeSH$$aMice, Knockout
000140709 650_2 $$2MeSH$$aSTAT5 Transcription Factor: metabolism
000140709 650_2 $$2MeSH$$aT-Lymphocytes, Regulatory: enzymology
000140709 650_2 $$2MeSH$$aT-Lymphocytes, Regulatory: immunology
000140709 7001_ $$aThabet, Yasser$$b1
000140709 7001_ $$aSchönfeld, Eva$$b2
000140709 7001_ $$0P:(DE-2719)2812698$$aKöhne, Maren$$b3$$udzne
000140709 7001_ $$aSommer, Daniel$$b4
000140709 7001_ $$aAbdullah, Zeinab$$b5
000140709 7001_ $$aSadlon, Timothy$$b6
000140709 7001_ $$0P:(DE-2719)2813660$$aOsei-Sarpong, Collins$$b7$$udzne
000140709 7001_ $$aSubbaramaiah, Kotha$$b8
000140709 7001_ $$aCopperi, Francesca$$b9
000140709 7001_ $$aHaendler, Kristian$$b10
000140709 7001_ $$0P:(DE-2719)2812488$$aVarga, Tamas$$b11$$udzne
000140709 7001_ $$aSchanz, Oliver$$b12
000140709 7001_ $$0P:(DE-2719)2811740$$aBourry, Svenja$$b13$$udzne
000140709 7001_ $$aBassler, Kevin$$b14
000140709 7001_ $$aKrebs, Wolfgang$$b15
000140709 7001_ $$aPeters, Annika E$$b16
000140709 7001_ $$aBaumgart, Ann-Kathrin$$b17
000140709 7001_ $$aSchneeweiss, Maria$$b18
000140709 7001_ $$aKlee, Kathrin$$b19
000140709 7001_ $$aSchmidt, Susanne V$$b20
000140709 7001_ $$aNüssing, Simone$$b21
000140709 7001_ $$aSander, Jil$$b22
000140709 7001_ $$aOhkura, Naganari$$b23
000140709 7001_ $$aWaha, Andreas$$b24
000140709 7001_ $$aSparwasser, Tim$$b25
000140709 7001_ $$aWunderlich, F Thomas$$b26
000140709 7001_ $$aFörster, Irmgard$$b27
000140709 7001_ $$0P:(DE-2719)9000845$$aUlas, Thomas$$b28$$udzne
000140709 7001_ $$aWeighardt, Heike$$b29
000140709 7001_ $$aSakaguchi, Shimon$$b30
000140709 7001_ $$aPfeifer, Alexander$$b31
000140709 7001_ $$aBlüher, Matthias$$b32
000140709 7001_ $$aDannenberg, Andrew J$$b33
000140709 7001_ $$aFerreirós, Nerea$$b34
000140709 7001_ $$aMuglia, Louis J$$b35
000140709 7001_ $$aWickenhauser, Claudia$$b36
000140709 7001_ $$aBarry, Simon C$$b37
000140709 7001_ $$0P:(DE-2719)2811660$$aSchultze, Joachim L$$b38$$udzne
000140709 7001_ $$0P:(DE-2719)2812219$$aBeyer, Marc$$b39$$eLast author$$udzne
000140709 77318 $$2Crossref$$3journal-article$$a10.1016/j.immuni.2019.03.014$$b : Elsevier BV, 2019-05-01$$n5$$p1232-1248.e14$$tImmunity$$v50$$x1074-7613$$y2019
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