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000906279 1001_ $$0P:(DE-HGF)0$$aXu, Haifeng C.$$b0
000906279 245__ $$aSingle MHC‐I Expression Promotes Virus‐Induced Liver Immunopathology
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000906279 520__ $$aMajor histocompatibility complex I (MHC-I) molecules present epitopes on the cellular surface of antigen-presenting cells to prime cytotoxic clusters of differentiation 8 (CD8)+ T cells (CTLs), which then identify and eliminate other cells such as virus-infected cells bearing the antigen. Human hepatitis virus cohort studies have previously identified MHC-I molecules as promising predictors of viral clearance. However, the underlying functional significance of these predictions is not fully understood. Here, we show that expression of single MHC-I isomers promotes virus-induced liver immunopathology. Specifically, using the lymphocytic choriomeningitis virus (LCMV) model system, we found MHC-I proteins to be highly up-regulated during infection. Deletion of one of the two MHC-I isomers histocompatibility antigen 2 (H2)–Db or H2-Kb in C57Bl/6 mice resulted in CTL activation recognizing the remaining MHC-I with LCMV epitopes in increased paucity. This increased CTL response resulted in hepatocyte death, increased caspase activation, and severe metabolic changes in liver tissue following infection with LCMV. Moreover, depletion of CTLs abolished LCMV-induced pathology in these mice with resulting viral persistence. In turn, natural killer (NK) cell depletion further increased antiviral CTL immunity and clearance of LCMV even in the presence of a single MHC-I isomer. Conclusion: Our results suggest that uniform MHC-I molecule expression promotes enhanced CTL immunity during viral infection and contributes to increased CTL-mediated liver cell damage that was alleviated by CD8 or NK cell depletion.
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000906279 7001_ $$0P:(DE-Juel1)185067$$aHuang, Jun$$b1
000906279 7001_ $$0P:(DE-HGF)0$$aPandyra, Aleksandra A.$$b2
000906279 7001_ $$0P:(DE-HGF)0$$aPandey, Piyush$$b3
000906279 7001_ $$0P:(DE-HGF)0$$aWang, Ruifeng$$b4
000906279 7001_ $$0P:(DE-HGF)0$$aZhang, Zeli$$b5
000906279 7001_ $$0P:(DE-HGF)0$$aZhuang, Yuan$$b6
000906279 7001_ $$0P:(DE-Juel1)174133$$aGertzen, Christoph G. W.$$b7
000906279 7001_ $$0P:(DE-HGF)0$$aMünk, Carsten$$b8
000906279 7001_ $$0P:(DE-HGF)0$$aHerebian, Diran$$b9
000906279 7001_ $$0P:(DE-HGF)0$$aBorkhardt, Arndt$$b10
000906279 7001_ $$0P:(DE-HGF)0$$aRecher, Mike$$b11
000906279 7001_ $$0P:(DE-Juel1)172663$$aGohlke, Holger$$b12
000906279 7001_ $$0P:(DE-HGF)0$$aEsposito, Irene$$b13
000906279 7001_ $$0P:(DE-HGF)0$$aOberbarnscheidt, Martin$$b14
000906279 7001_ $$0P:(DE-HGF)0$$aHäussinger, Dieter$$b15
000906279 7001_ $$0P:(DE-HGF)0$$aLang, Karl S.$$b16
000906279 7001_ $$0P:(DE-HGF)0$$aLang, Philipp A.$$b17$$eCorresponding author
000906279 773__ $$0PERI:(DE-600)2881134-3$$a10.1002/hep4.1913$$gp. hep4.1913$$n7$$p1620-1633$$tHepatology communications$$v6$$x2471-254X$$y2022
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