% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Schmidleithner:140709,
      author       = {Schmidleithner, Lisa and Thabet, Yasser and Schönfeld, Eva
                      and Köhne, Maren and Sommer, Daniel and Abdullah, Zeinab
                      and Sadlon, Timothy and Osei-Sarpong, Collins and
                      Subbaramaiah, Kotha and Copperi, Francesca and Haendler,
                      Kristian and Varga, Tamas and Schanz, Oliver and Bourry,
                      Svenja and Bassler, Kevin and Krebs, Wolfgang and Peters,
                      Annika E and Baumgart, Ann-Kathrin and Schneeweiss, Maria
                      and Klee, Kathrin and Schmidt, Susanne V and Nüssing,
                      Simone and Sander, Jil and Ohkura, Naganari and Waha,
                      Andreas and Sparwasser, Tim and Wunderlich, F Thomas and
                      Förster, Irmgard and Ulas, Thomas and Weighardt, Heike and
                      Sakaguchi, Shimon and Pfeifer, Alexander and Blüher,
                      Matthias and Dannenberg, Andrew J and Ferreirós, Nerea and
                      Muglia, Louis J and Wickenhauser, Claudia and Barry, Simon C
                      and Schultze, Joachim L and Beyer, Marc},
      title        = {{E}nzymatic {A}ctivity of {HPGD} in {T}reg {C}ells
                      {S}uppresses {T}conv {C}ells to {M}aintain {A}dipose
                      {T}issue {H}omeostasis and {P}revent {M}etabolic
                      {D}ysfunction.},
      journal      = {Immunity},
      volume       = {50},
      number       = {5},
      issn         = {1074-7613},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-07031},
      pages        = {1232-1248.e14},
      year         = {2019},
      abstract     = {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.},
      keywords     = {3T3 Cells / Animals / Cell Line / Diabetes Mellitus, Type
                      2: metabolism / Dinoprostone: analogs $\&$ derivatives /
                      Dinoprostone: metabolism / HEK293 Cells / Homeostasis:
                      immunology / Humans / Hydroxyprostaglandin Dehydrogenases:
                      genetics / Hydroxyprostaglandin Dehydrogenases: metabolism /
                      Insulin Resistance: genetics / Intra-Abdominal Fat: cytology
                      / Intra-Abdominal Fat: immunology / Jurkat Cells /
                      Lymphocyte Activation: immunology / Male / Mice / Mice,
                      Knockout / STAT5 Transcription Factor: metabolism /
                      T-Lymphocytes, Regulatory: enzymology / T-Lymphocytes,
                      Regulatory: immunology / STAT5 Transcription Factor (NLM
                      Chemicals) / 15-ketoprostaglandin E2 (NLM Chemicals) /
                      Hydroxyprostaglandin Dehydrogenases (NLM Chemicals) /
                      Dinoprostone (NLM Chemicals)},
      cin          = {AG Beyer / AG Alamoudi / Schultze - PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1013035 / I:(DE-2719)1013012 /
                      I:(DE-2719)1013031},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31027998},
      doi          = {10.1016/j.immuni.2019.03.014},
      url          = {https://pub.dzne.de/record/140709},
}