Cutting edge: STAT1-mediated epigenetic control of Rsad2 promotes clonal expansion of antiviral NK cells Journal Article


Authors: Wiedemann, G. M.; Geary, C. D.; Lau, C. M.; Sun, J. C.
Article Title: Cutting edge: STAT1-mediated epigenetic control of Rsad2 promotes clonal expansion of antiviral NK cells
Abstract: NK cells represent a cellular component of innate immunity but possess features of adaptive immunity, including clonal expansion and establishment of long-lived memory following infection. During mouse CMV (MCMV) infection, we observed Rsad2 (which encodes Viperin) to be among the most highly induced IFN stimulatory genes in activated NK cells, correlating with increased chromatin accessibility at the Rsad2 gene locus. Furthermore, in NK cells stimulated with IFN-a, the promoter region of Rsad2 was enriched for STAT1 binding and the permissive histone mark H3K4me3. IFN-aR– and STAT1-deficient NK cells showed an impairment of Rsad2 induction and chromatin accessibility during MCMV infection. Finally, Rsad2-deficient NK cells were defective in clonal expansion and memory formation following exposure to MCMV, in part because of greater apoptosis. Thus, our study reveals a critical mechanism of STAT1-mediated epigenetic control of Rsad2 to promote the adaptive behavior of NK cells during viral infection. Copyright © 2020 by The American Association of Immunologists, Inc. All rights reserved.
Journal Title: Journal of Immunology
Volume: 205
Issue: 1
ISSN: 0022-1767
Publisher: The American Association of Immunologists, Inc  
Date Published: 2020-07-01
Start Page: 21
End Page: 25
Language: English
DOI: 10.4049/jimmunol.2000086
PUBMED: 32461239
PROVIDER: scopus
PMCID: PMC7314649
DOI/URL:
Notes: Article -- Export Date: 3 August 2020 -- Source: Scopus
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MSK Authors
  1. Joseph C Sun
    94 Sun
  2. Clair   Geary
    13 Geary
  3. Colleen M Lau
    16 Lau