title: CD4-CD8-T cells contribute to the persistence of viral hepatitis by striking a delicate balance in immune modulation.
abstract: Viral hepatitis remains the most common cause of liver disease and a major public health problem. Here, we focus on the role of CD4 CD8 double negative T (DN T) cells involved in the mechanisms of viral persistence in hepatitis. C3H/HeJ mice infected with murine hepatitis virus strain 3 (MHV-3) were used to display chronic viral hepatitis. DN T cells dramatically increased in MHV-3 infected mice. Adoptive transfer of DN T cells from MHV-3 infected mice led to a significant increase in mice survival. The DN T cells with production of IFN-γ and IL-2 are able to kill virus-specific CD8(+) T cells via the Fas/FasL dependent pathway. The delicate balance of multiple effects of DN T cells may lead to viral persistence in MHV-3 induced hepatitis. In short, our study identified DN T cells contributing to viral persistence in MHV-3 induced hepatitis in C3H/HeJ mice, which provides a rationale for modulating DN T cells for the management of viral hepatitis.
authors.affiliation: Department of Infectious Disease and Institute of Infectious Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Xiaojing
authors.initials: X
authors.lastname: Wang
authors.forename: Weiming
authors.initials: W
authors.lastname: Yan
authors.forename: Yulei
authors.initials: Y
authors.lastname: Lu
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Ying
authors.initials: Y
authors.lastname: Sun
authors.forename: Xiaomin
authors.initials: X
authors.lastname: Qin
authors.forename: Jiangguo
authors.initials: J
authors.lastname: Zhang
authors.forename: Meifang
authors.initials: M
authors.lastname: Han
authors.forename: Wei
authors.initials: W
authors.lastname: Guo
authors.forename: Hongwu
authors.initials: H
authors.lastname: Wang
authors.forename: Di
authors.initials: D
authors.lastname: Wu
authors.forename: Dong
authors.initials: D
authors.lastname: Xi
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Luo
authors.forename: Qin
authors.initials: Q
authors.lastname: Ning
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D017209:Apoptosis; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000821:virology; D018352:Coronavirus Infections / Q000276:immunology* / Q000473:pathology; D003602:Cytotoxicity, Immunologic; D004195:Disease Models, Animal; D053222:Fas Ligand Protein / Q000502:physiology; D006521:Hepatitis, Chronic / Q000276:immunology / Q000473:pathology; D006524:Hepatitis, Viral, Animal / Q000276:immunology* / Q000473:pathology; D056747:Immunomodulation; D016130:Immunophenotyping; D008099:Liver / Q000473:pathology; D008222:Lymphokines / Q000378:metabolism; D051379:Mice; D008809:Mice, Inbred C3H; D006517:Murine hepatitis virus / Q000276:immunology*; D013154:Spleen / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism / Q000637:transplantation; D019014:fas Receptor / Q000502:physiology
chemical_list: D053222:Fas Ligand Protein; C491899:Fas protein, mouse; C505658:Fasl protein, mouse; D008222:Lymphokines; D019014:fas Receptor