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CCCH‐type zinc finger antiviral protein mediates antiviral immune response by activating T cells
Author(s) -
Zhu Mingjun,
Zhou Jing,
Liang Yanfei,
Nair Venugopal,
Yao Yongxiu,
Cheng Ziqiang
Publication year - 2020
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.1ab1119-314rrr
Subject(s) - biology , immune system , viral replication , virology , immunosuppression , t lymphocyte , immunology , virus , microbiology and biotechnology
The zinc finger antiviral protein (ZAP), as a host restriction factor, inhibits the replication of certain viruses by binding viral mRNA or proteins for degradation. However, little is known about the role of ZAP in the antiviral immune response. We now show that ZAP participates in the antiviral immune response by activating T cells. Overexpression of ZAP significantly inhibited avian leukosis virus subgroup J (ALV‐J) replication and reduced the associated inflammatory damage in vivo. In this study, we found that ZAP tended to be expressed in T lymphocytes, especially after ALV‐J infection. T lymphocyte proliferation proceeded as usual in response to ALV‐J infection in the presence of ZAP, indicating that ZAP endows T lymphocytes with resistance to the immunosuppression caused by ALV‐J. Furthermore, ZAP activated cytokine secretion by T lymphocytes by contributing to nuclear translocation of nuclear factors of activated T cells and indirectly promoted anti‐ALV‐J antibody generation. Together, our findings show that ZAP, acting as an immunomodulatory factor, is involved in the antiviral immune response via T lymphocyte activation.