PMID- 31720044
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1598-2629 (Print)
IS  - 2092-6685 (Electronic)
IS  - 1598-2629 (Linking)
VI  - 19
IP  - 5
DP  - 2019 Oct
TI  - Viperin Differentially Induces Interferon-Stimulated Genes in Distinct Cell 
      Types.
PG  - e33
LID - 10.4110/in.2019.19.e33 [doi]
LID - e33
AB  - Viperin is an IFN-stimulated gene (ISG)-encoded protein that was identified in 
      human primary macrophages treated with IFN-gamma and in human primary fibroblasts 
      infected with cytomegalovirus (CMV). This protein plays multiple roles in various 
      cell types. It inhibits viral replication, mediates signaling pathways, and 
      regulates cellular metabolism. Recent studies have shown that viperin inhibits 
      IFN expression in macrophages, while it enhances TLR7 and TLR9-mediated IFN 
      production in plasmacytoid dendritic cells, suggesting that viperin can play 
      different roles in activation of the same pathway in different cell types. 
      Viperin also controls induction of ISGs in macrophages. However, the effect of 
      viperin on induction of ISGs in cell types other than macrophages is unknown. 
      Here, we show that viperin differentially induces ISGs in 2 distinct cell types, 
      macrophages and fibroblasts isolated from wild type and viperin knockout mice. 
      Unlike in bone marrow-derived macrophages (BMDMs), viperin downregulates the 
      expression levels of ISGs such as bone marrow stromal cell antigen-2, Isg15, 
      Isg54, myxovirus resistance dynamin like GTPase 2, and guanylate binding protein 
      2 in murine embryonic fibroblasts (MEFs) treated with type I or II IFN. However, 
      viperin upregulates expression of these ISGs in both BMDMs and MEFs stimulated 
      with polyinosinic-polycytidylic acid or CpG DNA and infected with murine CMV. The 
      efficiency of viral entry is inversely proportional to the expression levels of 
      ISGs in both cell types. The data indicate that viperin differentially regulates 
      induction of ISGs in a cell type-dependent manner, which might provide different 
      innate immune responses in distinct cell types against infections.
CI  - Copyright (c) 2019. The Korean Association of Immunologists.
FAU - Kim, Jeong Jin
AU  - Kim JJ
AD  - Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical 
      Science, Yonsei University College of Medicine, Seoul 03722, Korea.
FAU - Kim, Ku Sul
AU  - Kim KS
AD  - Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical 
      Science, Yonsei University College of Medicine, Seoul 03722, Korea.
FAU - Eom, John
AU  - Eom J
AD  - Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical 
      Science, Yonsei University College of Medicine, Seoul 03722, Korea.
FAU - Lee, Jae Bong
AU  - Lee JB
AD  - Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical 
      Science, Yonsei University College of Medicine, Seoul 03722, Korea.
FAU - Seo, Jun-Young
AU  - Seo JY
AUID- ORCID: 0000-0003-4004-2013
AD  - Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical 
      Science, Yonsei University College of Medicine, Seoul 03722, Korea.
LA  - eng
PT  - Journal Article
DEP - 20191004
PL  - Korea (South)
TA  - Immune Netw
JT  - Immune network
JID - 101137270
PMC - PMC6829070
OTO - NOTNLM
OT  - Cytomegalovirus
OT  - Fibroblasts
OT  - ISG
OT  - Interferons
OT  - Macrophages
OT  - Viperin
COIS- Conflict of Interest: The authors declare no potential conflicts of interest.
EDAT- 2019/11/14 06:00
MHDA- 2019/11/14 06:01
PMCR- 2019/10/01
CRDT- 2019/11/14 06:00
PHST- 2019/09/02 00:00 [received]
PHST- 2019/09/16 00:00 [revised]
PHST- 2019/09/18 00:00 [accepted]
PHST- 2019/11/14 06:00 [entrez]
PHST- 2019/11/14 06:00 [pubmed]
PHST- 2019/11/14 06:01 [medline]
PHST- 2019/10/01 00:00 [pmc-release]
AID - 2019190504 [pii]
AID - 10.4110/in.2019.19.e33 [doi]
PST - epublish
SO  - Immune Netw. 2019 Oct 4;19(5):e33. doi: 10.4110/in.2019.19.e33. eCollection 2019 
      Oct.