The proapoptotic Bcl-2 family member Bim plays a central role during the development of virus-induced hepatitis

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2012
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Lauer, Christoph
Corazza, Nadia
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The Journal of Immunology ; 188 (2012), 2. - pp. 916-922. - ISSN 0022-1767. - eISSN 1550-6606
Abstract
The proapoptotic Bcl-2 homolog Bim was shown to control the apoptosis of both T cells and hepatocytes. This dual role of Bim might be particularly relevant for the development of viral hepatitis, in which both the sensitivity of hepatocytes to apoptosis stimuli and the persistence of cytotoxic T cells are essential factors for the outcome of the disease. The relevance of Bim in regulating survival of cytotoxic T cells or induction of hepatocyte death has only been investigated in separate systems, and their relative contributions to the pathogenesis of T cell-mediated hepatitis remain unclear. Using the highly dynamic model system of lymphocytic choriomeningitis virus-mediated hepatitis and bone marrow chimeras, we found that Bim has a dual role in the development of lymphocytic choriomeningitis virus-induced, T cell-mediated hepatitis. Although the absence of Bim in parenchymal cells led to markedly attenuated liver damage, loss of Bim in the lymphoid compartment moderately enhanced hepatitis. However, when both effects were combined in Bim2/2 mice, the effect of Bim deficiency in the lymphoid compartment was overcompensated for by the reduced sensitivity of Bim2/2 hepatocytes to T cell-induced apoptosis, resulting in the protection of Bim2/2 mice from hepatitis.
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ISO 690LAUER, Christoph, Thomas BRUNNER, Nadia CORAZZA, 2012. The proapoptotic Bcl-2 family member Bim plays a central role during the development of virus-induced hepatitis. In: The Journal of Immunology. 188(2), pp. 916-922. ISSN 0022-1767. eISSN 1550-6606. Available under: doi: 10.4049/jimmunol.1101864
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@article{Lauer2012-01-15proap-18111,
  year={2012},
  doi={10.4049/jimmunol.1101864},
  title={The proapoptotic Bcl-2 family member Bim plays a central role during the development of virus-induced hepatitis},
  number={2},
  volume={188},
  issn={0022-1767},
  journal={The Journal of Immunology},
  pages={916--922},
  author={Lauer, Christoph and Brunner, Thomas and Corazza, Nadia}
}
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    <dcterms:abstract xml:lang="eng">The proapoptotic Bcl-2 homolog Bim was shown to control the apoptosis of both T cells and hepatocytes. This dual role of Bim might be particularly relevant for the development of viral hepatitis, in which both the sensitivity of hepatocytes to apoptosis stimuli and the persistence of cytotoxic T cells are essential factors for the outcome of the disease. The relevance of Bim in regulating survival of cytotoxic T cells or induction of hepatocyte death has only been investigated in separate systems, and their relative contributions to the pathogenesis of T cell-mediated hepatitis remain unclear. Using the highly dynamic model system of lymphocytic choriomeningitis virus-mediated hepatitis and bone marrow chimeras, we found that Bim has a dual role in the development of lymphocytic choriomeningitis virus-induced, T  cell-mediated hepatitis. Although the absence of Bim in parenchymal cells led to markedly attenuated liver damage, loss of Bim in the lymphoid compartment moderately enhanced hepatitis. However, when both effects were combined in Bim2/2 mice, the effect of Bim deficiency in the lymphoid compartment was overcompensated for by the reduced sensitivity of Bim2/2 hepatocytes to T cell-induced apoptosis, resulting in the protection of Bim2/2 mice from hepatitis.</dcterms:abstract>
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