Abstract：
:The mechanisms of each subset of immune cells contributing to the pathogenesis of viral hepatitis remain incompletely understood. In this study, we examined the role of liver CD4(-) CD8(-) (double negative, DN) T cells during murine hepatitis virus strain 3 (MHV-3)-induced hepatitis in C3H/HeJ mice. We demonstrate that predominant population of DN T cells in the liver of healthy or MHV-3-infected mice express TCRγδ(+). The proportion of TCRγδ(+) DN T cells in liver CD3(+) T cells was markedly increased after MHV-3 infection. Adoptive transfer of TCRγδ(+) DN T cells led to dramatically decreased survival in MHV-3-infected mice, accompanied by deteriorated histopathology and elevated ALT and AST levels. It was found that these cells were hyperactivated after MHV-3 infection with a production of TNF-α, IFN-γ, IL-2 and IL-17A. Highly activated liver TCRγδ(+) DN T cells were cytotoxic to MHV-3-infected hepatocytes in vitro and this effect did not require cell-cell contact. Moreover, the cytotoxic effect of liver TCRγδ(+) DN T cells against hepatocytes involves TNF-α pathway, but not IL-17A or IFN-γ. These results indicate that liver TCRγδ(+) DN T cells play a critical role in the liver injury in MHV-3-induced hepatitis, via a TNF-α dependent pathway.
journal_name
Mol Immunoljournal_title
Molecular immunologyauthors
Lu Y,Wang X,Yan W,Wang H,Wang M,Wu D,Zhu L,Luo X,Ning Qdoi
10.1016/j.molimm.2012.05.017subject
Has Abstractpub_date
2012-10-01 00:00:00pages
229-36issue
3-4eissn
0161-5890issn
1872-9142pii
S0161-5890(12)00318-5journal_volume
52pub_type
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