Abstract:
:Autoimmune hepatitis (AIH) is a chronic liver disease mediated by immunity, and could lead to liver fibrosis and hepatocellular carcinoma. However, the mechanisms for breaking hepatic tolerance and driving AIH still remain elusive. We herein reported that the non-specific liver inflammation triggered by carbon tetrachloride (CCl4) recruited high numbers of CD4+T, CD8+T and B cells, and elevated the expression of proinflammaitory cytokines in Balb/c mice, further breaking liver tolerance and inducing autoimmune response, AIH inflammation and liver fibrosis in the presence of CYP2D6 antigen mimicry. In contrast, adenovirus infection could not break liver tolerance and induce AIH in Balb/c mice even in the presence of CYP2D6 antigen mimicry. These results suggested that genetic predisposition could determine liver tolerance in Balb/c mice. The chemical induced inflammation in the liver breaks tolerance and might be considered important for the initiation and development of AIH in Balb/c mice.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Chi G,Pei JH,Ma QY,Ru YX,Feng ZHdoi
10.1016/j.imlet.2019.11.010subject
Has Abstractpub_date
2020-02-01 00:00:00pages
44-50eissn
0165-2478issn
1879-0542pii
S0165-2478(19)30395-5journal_volume
218pub_type
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