NKG2A is a NK cell exhaustion checkpoint for HCV persistence View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Chao Zhang, Xiao-mei Wang, Shu-ran Li, Trix Twelkmeyer, Wei-hong Wang, Sheng-yuan Zhang, Shu-feng Wang, Ji-zheng Chen, Xia Jin, Yu-zhang Wu, Xin-wen Chen, Sheng-dian Wang, Jun-qi Niu, Hai-rong Chen, Hong Tang

ABSTRACT

Exhaustion of cytotoxic effector natural killer (NK) and CD8+ T cells have important functions in the establishment of persistent viral infections, but how exhaustion is induced during chronic hepatitis C virus (HCV) infection remains poorly defined. Here we show, using the humanized C/OTg mice permissive for persistent HCV infection, that NK and CD8+ T cells become sequentially exhausted shortly after their transient hepatic infiltration and activation in acute HCV infection. HCV infection upregulates Qa-1 expression in hepatocytes, which ligates NKG2A to induce NK cell exhaustion. Antibodies targeting NKG2A or Qa-1 prevents NK exhaustion and promotes NK-dependent HCV clearance. Moreover, reactivated NK cells provide sufficient IFN-γ that helps rejuvenate polyclonal HCV CD8+ T cell response and clearance of HCV. Our data thus show that NKG2A serves as a critical checkpoint for HCV-induced NK exhaustion, and that NKG2A blockade sequentially boosts interdependent NK and CD8+ T cell functions to prevent persistent HCV infection. More... »

PAGES

1507

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-019-09212-y

    DOI

    http://dx.doi.org/10.1038/s41467-019-09212-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1113182123

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30944315


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