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@ARTICLE{Xu:906279,
      author       = {Xu, Haifeng C. and Huang, Jun and Pandyra, Aleksandra A.
                      and Pandey, Piyush and Wang, Ruifeng and Zhang, Zeli and
                      Zhuang, Yuan and Gertzen, Christoph G. W. and Münk, Carsten
                      and Herebian, Diran and Borkhardt, Arndt and Recher, Mike
                      and Gohlke, Holger and Esposito, Irene and Oberbarnscheidt,
                      Martin and Häussinger, Dieter and Lang, Karl S. and Lang,
                      Philipp A.},
      title        = {{S}ingle {MHC}‐{I} {E}xpression {P}romotes
                      {V}irus‐{I}nduced {L}iver {I}mmunopathology},
      journal      = {Hepatology communications},
      volume       = {6},
      number       = {7},
      issn         = {2471-254X},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {FZJ-2022-01343},
      pages        = {1620-1633},
      year         = {2022},
      abstract     = {Major histocompatibility complex I (MHC-I) molecules
                      present epitopes on the cellular surface of
                      antigen-presenting cells to prime cytotoxic clusters of
                      differentiation 8 (CD8)+ T cells (CTLs), which then identify
                      and eliminate other cells such as virus-infected cells
                      bearing the antigen. Human hepatitis virus cohort studies
                      have previously identified MHC-I molecules as promising
                      predictors of viral clearance. However, the underlying
                      functional significance of these predictions is not fully
                      understood. Here, we show that expression of single MHC-I
                      isomers promotes virus-induced liver immunopathology.
                      Specifically, using the lymphocytic choriomeningitis virus
                      (LCMV) model system, we found MHC-I proteins to be highly
                      up-regulated during infection. Deletion of one of the two
                      MHC-I isomers histocompatibility antigen 2 (H2)–Db or
                      H2-Kb in C57Bl/6 mice resulted in CTL activation recognizing
                      the remaining MHC-I with LCMV epitopes in increased paucity.
                      This increased CTL response resulted in hepatocyte death,
                      increased caspase activation, and severe metabolic changes
                      in liver tissue following infection with LCMV. Moreover,
                      depletion of CTLs abolished LCMV-induced pathology in these
                      mice with resulting viral persistence. In turn, natural
                      killer (NK) cell depletion further increased antiviral CTL
                      immunity and clearance of LCMV even in the presence of a
                      single MHC-I isomer. Conclusion: Our results suggest that
                      uniform MHC-I molecule expression promotes enhanced CTL
                      immunity during viral infection and contributes to increased
                      CTL-mediated liver cell damage that was alleviated by CD8 or
                      NK cell depletion.},
      cin          = {JSC / IBI-7 / NIC / IBG-4},
      ddc          = {610},
      cid          = {I:(DE-Juel1)JSC-20090406 / I:(DE-Juel1)IBI-7-20200312 /
                      I:(DE-Juel1)NIC-20090406 / I:(DE-Juel1)IBG-4-20200403},
      pnm          = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
                      (SDLs) and Research Groups (POF4-511) / 5241 - Molecular
                      Information Processing in Cellular Systems (POF4-524) /
                      Forschergruppe Gohlke $(hkf7_20200501)$},
      pid          = {G:(DE-HGF)POF4-5111 / G:(DE-HGF)POF4-5241 /
                      $G:(DE-Juel1)hkf7_20200501$},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35166071},
      UT           = {WOS:000754878800001},
      doi          = {10.1002/hep4.1913},
      url          = {https://juser.fz-juelich.de/record/906279},
}