期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 168, 期 4, 页码 1169-1178出版社
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2006.050875
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资金
- NIAID NIH HHS [T32-AI-07285, K08-AI-055888, T32 AI007285, R01 AI037554, K08 AI055888, R01-AI-037554] Funding Source: Medline
- NIA NIH HHS [P30 AG018254, R01 AG021970, R01-AG-021970, P30-AG18254] Funding Source: Medline
- NIEHS NIH HHS [ES-01247] Funding Source: Medline
Respiratory infections, including influenza in humans, are often accompanied by a hepatitis that is usually mild and self-limiting. The mechanism of this kind of liver damage is not well understood. in the present study, we show that influenza-associated hepatitis occurs due to the formation of inflammatory foci that include apoptotic hepatocytes, antigen-specific CD8(+) T cells, and Kupffer cells. Serum aminotransaminase levels were elevated, and both the histological and serum enzyme markers of hepatitis were increased in secondary influenza infection, consistent with a primary role for antigen-specific T cells in the pathogenesis. No virus could be detected in the liver, making this a pure example of collateral damage of the liver. Notably, removal of the Kupffer cells prevented the hepatitis. Such hepatic collateral damage may be a general consequence of expanding CD8(+) T-cell populations during many extrahepatic viral infections, yielding important implications for liver pathobiology.
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