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@ARTICLE{ToVinh:164086,
      author       = {ToVinh, Michael and Hörr, Gregor and Dobrikova, Kristiyana
                      and Gotter, Christina and Rommel, Clemens and Hoffmeister,
                      Christoph and Raabe, Jan and Kaiser, Kim M and Finnemann,
                      Claudia and Bischoff, Jenny and Rieke, Gereon J and Wilhelm,
                      Christoph and Schmitt, Vanessa and Möhl, Christoph and
                      Aghabeig, Mansoureh and Schwarze-Zander, Carolynne and
                      Boesecke, Christoph and van Bremen, Kathrin and Wasmuth,
                      Jan-Christian and Strassburg, Christian P and Rockstroh,
                      Jürgen K and Spengler, Ulrich and Krämer, Benjamin and
                      Nattermann, Jacob},
      title        = {{M}itochondrial dysfunction contributes to impaired
                      cytokine production of {CD}56 bright {NK} cells from
                      {HIV}(+) individuals under effective antiviral therapy.},
      journal      = {The journal of infectious diseases},
      volume       = {226},
      number       = {5},
      issn         = {0022-1899},
      address      = {Oxford [u.a.]},
      publisher    = {Oxford Univ. Press},
      reportid     = {DZNE-2022-00749},
      pages        = {901-906},
      year         = {2022},
      abstract     = {HIV infection is associated with impaired NK cell activity,
                      which is only incompletely restored under antiretroviral
                      therapy. Analysing the bioenergetics profiles of oxygen
                      consumption, we observed several parameters were
                      significantly reduced in HIV(+) NK cells, indicating a
                      mitochondrial defect. Accordingly, we found HIV(+) CD56
                      bright NK cells to display a decreased mitochondrial
                      membrane potential and mitochondrial mass. Both parameters
                      were positively correlated with IFNγ production of NK
                      cells. Finally, we demonstrated that stimulation of HIV(+)
                      NK cells with MitoTEMPO, mitochondria-targeting antioxidant,
                      significantly improved IFNγ production. In conclusion, we
                      identified mitochondrial dysfunction as a mechanism that
                      contributes to impaired NK cell function.},
      keywords     = {HIV (Other) / IFNγ (Other) / NK cell (Other) /
                      immunometabolism (Other) / mitochondrial dysfunction
                      (Other)},
      cin          = {IDAF},
      ddc          = {610},
      cid          = {I:(DE-2719)1040200},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      experiment   = {EXP:(DE-2719)IDAF-20190308},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35313340},
      doi          = {10.1093/infdis/jiac103},
      url          = {https://pub.dzne.de/record/164086},
}