Lauer, Christoph; Brunner, Thomas; Corazza, Nadia (2012). The proapoptotic Bcl-2 family member Bim plays a central role during the development of virus-induced hepatitis. Journal of immunology, 188(2), pp. 916-22. Bethesda, Md.: American Association of Immunologists 10.4049/jimmunol.1101864
Full text not available from this repository. (Request a copy)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 Bim(-/-) mice, the effect of Bim deficiency in the lymphoid compartment was overcompensated for by the reduced sensitivity of Bim(-/-) hepatocytes to T cell-induced apoptosis, resulting in the protection of Bim(-/-) mice from hepatitis.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute of Pathology |
UniBE Contributor: |
Corazza, Nadia |
ISSN: |
0022-1767 |
Publisher: |
American Association of Immunologists |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:24 |
Last Modified: |
05 Dec 2022 14:07 |
Publisher DOI: |
10.4049/jimmunol.1101864 |
PubMed ID: |
22156338 |
Web of Science ID: |
000299323700046 |
URI: |
https://boris.unibe.ch/id/eprint/8565 (FactScience: 214151) |
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