guest ::
| Home > Publications database > Single MHC‐I Expression Promotes Virus‐Induced Liver Immunopathology > print |
| Home > Publications database > Single MHC‐I Expression Promotes Virus‐Induced Liver Immunopathology > print |
| 001 | 906279 | ||
| 005 | 20230128125811.0 | ||
| 024 | 7 | _ | |a 10.1002/hep4.1913 |2 doi |
| 024 | 7 | _ | |a 2128/31378 |2 Handle |
| 024 | 7 | _ | |a altmetric:123096698 |2 altmetric |
| 024 | 7 | _ | |a pmid:35166071 |2 pmid |
| 024 | 7 | _ | |a WOS:000754878800001 |2 WOS |
| 037 | _ | _ | |a FZJ-2022-01343 |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Xu, Haifeng C. |0 P:(DE-HGF)0 |b 0 |
| 245 | _ | _ | |a Single MHC‐I Expression Promotes Virus‐Induced Liver Immunopathology |
| 260 | _ | _ | |a Hoboken, NJ |c 2022 |b Wiley |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1674828969_23946 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a 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. |
| 536 | _ | _ | |a 5111 - Domain-Specific Simulation & Data Life Cycle Labs (SDLs) and Research Groups (POF4-511) |0 G:(DE-HGF)POF4-5111 |c POF4-511 |f POF IV |x 0 |
| 536 | _ | _ | |a 5241 - Molecular Information Processing in Cellular Systems (POF4-524) |0 G:(DE-HGF)POF4-5241 |c POF4-524 |f POF IV |x 1 |
| 536 | _ | _ | |a Forschergruppe Gohlke (hkf7_20200501) |0 G:(DE-Juel1)hkf7_20200501 |c hkf7_20200501 |f Forschergruppe Gohlke |x 2 |
| 588 | _ | _ | |a Dataset connected to CrossRef, Journals: juser.fz-juelich.de |
| 700 | 1 | _ | |a Huang, Jun |0 P:(DE-Juel1)185067 |b 1 |
| 700 | 1 | _ | |a Pandyra, Aleksandra A. |0 P:(DE-HGF)0 |b 2 |
| 700 | 1 | _ | |a Pandey, Piyush |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Wang, Ruifeng |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Zhang, Zeli |0 P:(DE-HGF)0 |b 5 |
| 700 | 1 | _ | |a Zhuang, Yuan |0 P:(DE-HGF)0 |b 6 |
| 700 | 1 | _ | |a Gertzen, Christoph G. W. |0 P:(DE-Juel1)174133 |b 7 |
| 700 | 1 | _ | |a Münk, Carsten |0 P:(DE-HGF)0 |b 8 |
| 700 | 1 | _ | |a Herebian, Diran |0 P:(DE-HGF)0 |b 9 |
| 700 | 1 | _ | |a Borkhardt, Arndt |0 P:(DE-HGF)0 |b 10 |
| 700 | 1 | _ | |a Recher, Mike |0 P:(DE-HGF)0 |b 11 |
| 700 | 1 | _ | |a Gohlke, Holger |0 P:(DE-Juel1)172663 |b 12 |
| 700 | 1 | _ | |a Esposito, Irene |0 P:(DE-HGF)0 |b 13 |
| 700 | 1 | _ | |a Oberbarnscheidt, Martin |0 P:(DE-HGF)0 |b 14 |
| 700 | 1 | _ | |a Häussinger, Dieter |0 P:(DE-HGF)0 |b 15 |
| 700 | 1 | _ | |a Lang, Karl S. |0 P:(DE-HGF)0 |b 16 |
| 700 | 1 | _ | |a Lang, Philipp A. |0 P:(DE-HGF)0 |b 17 |e Corresponding author |
| 773 | _ | _ | |a 10.1002/hep4.1913 |g p. hep4.1913 |0 PERI:(DE-600)2881134-3 |n 7 |p 1620-1633 |t Hepatology communications |v 6 |y 2022 |x 2471-254X |
| 856 | 4 | _ | |u https://juser.fz-juelich.de/record/906279/files/Hepatology%20Communications%20-%202022%20-%20Xu%20-%20Single%20MHC%E2%80%90I%20Expression%20Promotes%20Virus%E2%80%90Induced%20Liver%20Immunopathology.pdf |y OpenAccess |
| 856 | 4 | _ | |u https://juser.fz-juelich.de/record/906279/files/Xu%20et%20al_hep%20Com_rev2.pdf |y OpenAccess |
| 856 | 4 | _ | |u https://juser.fz-juelich.de/record/906279/files/Xu%20et%20al_hep%20Com_revision_R2.pdf |y Restricted |
| 909 | C | O | |o oai:juser.fz-juelich.de:906279 |p openaire |p open_access |p VDB |p driver |p dnbdelivery |
| 910 | 1 | _ | |a Forschungszentrum Jülich |0 I:(DE-588b)5008462-8 |k FZJ |b 7 |6 P:(DE-Juel1)174133 |
| 910 | 1 | _ | |a Forschungszentrum Jülich |0 I:(DE-588b)5008462-8 |k FZJ |b 12 |6 P:(DE-Juel1)172663 |
| 913 | 1 | _ | |a DE-HGF |b Key Technologies |l Engineering Digital Futures – Supercomputing, Data Management and Information Security for Knowledge and Action |1 G:(DE-HGF)POF4-510 |0 G:(DE-HGF)POF4-511 |3 G:(DE-HGF)POF4 |2 G:(DE-HGF)POF4-500 |4 G:(DE-HGF)POF |v Enabling Computational- & Data-Intensive Science and Engineering |9 G:(DE-HGF)POF4-5111 |x 0 |
| 913 | 1 | _ | |a DE-HGF |b Key Technologies |l Natural, Artificial and Cognitive Information Processing |1 G:(DE-HGF)POF4-520 |0 G:(DE-HGF)POF4-524 |3 G:(DE-HGF)POF4 |2 G:(DE-HGF)POF4-500 |4 G:(DE-HGF)POF |v Molecular and Cellular Information Processing |9 G:(DE-HGF)POF4-5241 |x 1 |
| 914 | 1 | _ | |y 2022 |
| 915 | _ | _ | |a Creative Commons Attribution-NonCommercial-NoDerivs CC BY-NC-ND 4.0 |0 LIC:(DE-HGF)CCBYNCND4 |2 HGFVOC |
| 915 | _ | _ | |a Fees |0 StatID:(DE-HGF)0700 |2 StatID |d 2020-08-32 |
| 915 | _ | _ | |a OpenAccess |0 StatID:(DE-HGF)0510 |2 StatID |
| 915 | _ | _ | |a Article Processing Charges |0 StatID:(DE-HGF)0561 |2 StatID |d 2020-08-32 |
| 915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b HEPATOL COMMUN : 2021 |d 2022-11-09 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0200 |2 StatID |b SCOPUS |d 2022-11-09 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0300 |2 StatID |b Medline |d 2022-11-09 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0501 |2 StatID |b DOAJ Seal |d 2021-04-16T15:13:23Z |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0500 |2 StatID |b DOAJ |d 2021-04-16T15:13:23Z |
| 915 | _ | _ | |a Peer Review |0 StatID:(DE-HGF)0030 |2 StatID |b DOAJ : Blind peer review |d 2021-04-16T15:13:23Z |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0199 |2 StatID |b Clarivate Analytics Master Journal List |d 2022-11-09 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0150 |2 StatID |b Web of Science Core Collection |d 2022-11-09 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1110 |2 StatID |b Current Contents - Clinical Medicine |d 2022-11-09 |
| 915 | _ | _ | |a IF >= 5 |0 StatID:(DE-HGF)9905 |2 StatID |b HEPATOL COMMUN : 2021 |d 2022-11-09 |
| 920 | _ | _ | |l yes |
| 920 | 1 | _ | |0 I:(DE-Juel1)JSC-20090406 |k JSC |l Jülich Supercomputing Center |x 0 |
| 920 | 1 | _ | |0 I:(DE-Juel1)IBI-7-20200312 |k IBI-7 |l Strukturbiochemie |x 1 |
| 920 | 1 | _ | |0 I:(DE-Juel1)NIC-20090406 |k NIC |l John von Neumann - Institut für Computing |x 2 |
| 920 | 1 | _ | |0 I:(DE-Juel1)IBG-4-20200403 |k IBG-4 |l Bioinformatik |x 3 |
| 980 | _ | _ | |a journal |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a I:(DE-Juel1)JSC-20090406 |
| 980 | _ | _ | |a I:(DE-Juel1)IBI-7-20200312 |
| 980 | _ | _ | |a I:(DE-Juel1)NIC-20090406 |
| 980 | _ | _ | |a I:(DE-Juel1)IBG-4-20200403 |
| 980 | _ | _ | |a UNRESTRICTED |
| 980 | 1 | _ | |a FullTexts |
| Library | Collection | CLSMajor | CLSMinor | Language | Author |
|---|