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@ARTICLE{Coe:164565,
      author       = {Coe, David and Poobalasingam, Thanushiyan and Fu, Hongmei
                      and Bonacina, Fabrizia and Wang, Guosu and Morales, Valle
                      and Moregola, Annalisa and Mitro, Nico and Cheung, Kenneth
                      Cp and Ward, Eleanor J and Nadkarni, Suchita and
                      Aksentijevic, Dunja and Bianchi, Katiuscia and Norata,
                      Giuseppe Danilo and Capasso, Melania and Federica,
                      Marelli-Berg},
      title        = {{L}oss of voltage-gated hydrogen channel 1 expression
                      reveals heterogeneous metabolic adaptation to intracellular
                      acidification by {T} cells.},
      journal      = {JCI insight},
      volume       = {7},
      number       = {10},
      issn         = {2379-3708},
      address      = {Ann Arbor, Michigan},
      publisher    = {JCI Insight},
      reportid     = {DZNE-2022-01114},
      pages        = {e147814},
      year         = {2022},
      note         = {(CC BY 4.0)},
      abstract     = {Voltage-gated hydrogen channel 1 (Hvcn1) is a voltage-gated
                      proton channel, which reduces cytosol acidification and
                      facilitates the production of ROS. The increased expression
                      of this channel in some cancers has led to proposing Hvcn1
                      antagonists as potential therapeutics. While its role in
                      most leukocytes has been studied in depth, the function of
                      Hvcn1 in T cells remains poorly defined. We show that Hvcn1
                      plays a nonredundant role in protecting naive T cells from
                      intracellular acidification during priming. Despite sharing
                      overall functional impairment in vivo and in vitro,
                      Hvcn1-deficient CD4+ and CD8+ T cells display profound
                      differences during the transition from naive to primed T
                      cells, including in the preservation of T cell receptor
                      (TCR) signaling, cellular division, and death. These
                      selective features result, at least in part, from a
                      substantially different metabolic response to intracellular
                      acidification associated with priming. While Hvcn1-deficient
                      naive CD4+ T cells reprogram to rescue the glycolytic
                      pathway, naive CD8+ T cells, which express high levels of
                      this channel in the mitochondria, respond by metabolically
                      compensating mitochondrial dysfunction, at least in part via
                      AMPK activation. These observations imply heterogeneity
                      between adaptation of naive CD4+ and CD8+ T cells to
                      intracellular acidification during activation.},
      keywords     = {Hydrogen / Hydrogen-Ion Concentration / Lymphocyte Count /
                      Protons / Signal Transduction / Adaptive immunity (Other) /
                      Immunology (Other) / Protons (NLM Chemicals) / Hydrogen (NLM
                      Chemicals)},
      cin          = {AG Capasso},
      ddc          = {610},
      cid          = {I:(DE-2719)1013033},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9220931},
      pubmed       = {pmid:35472029},
      doi          = {10.1172/jci.insight.147814},
      url          = {https://pub.dzne.de/record/164565},
}