PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

MCPIP1 is a positive regulator of type I interferons antiviral activity.

Abstract Type-I interferons (IFN-I) are widely used for antiviral immunotherapy in clinic. Therefore, identification of the regulators of IFN-I antiviral activity is important for developing novel targets for IFN-based antiviral therapy. Monocyte chemoattractant protein 1-induced protein 1 (MCPIP1) is critical for cellular inflammatory responses. However, the roles of MCPIP1 in interferons (IFNs)-mediated antiviral immunity are unexplored. In this study, we demonstrate for the first time that MCPIP1 is an important positive regulator of IFNs antiviral activity. We found that MCPIP1 can promote innate antiviral immunity independently of both its RNase and deubiquitinase activity. Furthermore, we reveal that MCPIP1 is an IFN-induced positive feedback signal molecule which promotes IFN-I-mediated antiviral efficacy. Mechanistically, MCPIP1 does not affect the activation of JAK/STAT upstream of IFN-I signaling, but significantly promotes IFN-I signaling by enhancing ISRE promoter activity and expression of interferon-stimulated genes (ISGs). And MCPIP1-mediated activation of IFN-I signaling is independently of its RNase and deubiquitinase activity. These findings uncover a novel innate antiviral mechanism mediated by the IFN-MCPIP1 axis, and may provide potential targets for enhancing IFNs antiviral therapy.
PMID
Related Publications

Human Cytokinome Analysis for Interferon Response.

Regulation of the transcriptional activity of the IRF7 promoter by a pathway independent of interferon signaling.

Regulation of antiviral innate immunity by deubiquitinase CYLD.

Inducible microRNA-155 feedback promotes type I IFN signaling in antiviral innate immunity by targeting suppressor of cytokine signaling 1.

MicroRNA-223 Promotes Type I Interferon Production in Antiviral Innate Immunity by Targeting Forkhead Box Protein O3 (FOXO3).

Authors

Mayor MeshTerms

Immunity, Innate

Keywords

Antiviral activity

ISGs

ISRE

Interferon

MCPIP1

Journal Title biochemical and biophysical research communications
Publication Year Start




PMID- 29545178
OWN - NLM
STAT- MEDLINE
DCOM- 20180413
LR  - 20180413
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 498
IP  - 4
DP  - 2018 Apr 15
TI  - MCPIP1 is a positive regulator of type I interferons antiviral activity.
PG  - 891-897
LID - S0006-291X(18)30562-X [pii]
LID - 10.1016/j.bbrc.2018.03.076 [doi]
AB  - Type-I interferons (IFN-I) are widely used for antiviral immunotherapy in clinic.
      Therefore, identification of the regulators of IFN-I antiviral activity is
      important for developing novel targets for IFN-based antiviral therapy. Monocyte 
      chemoattractant protein 1-induced protein 1 (MCPIP1) is critical for cellular
      inflammatory responses. However, the roles of MCPIP1 in interferons
      (IFNs)-mediated antiviral immunity are unexplored. In this study, we demonstrate 
      for the first time that MCPIP1 is an important positive regulator of IFNs
      antiviral activity. We found that MCPIP1 can promote innate antiviral immunity
      independently of both its RNase and deubiquitinase activity. Furthermore, we
      reveal that MCPIP1 is an IFN-induced positive feedback signal molecule which
      promotes IFN-I-mediated antiviral efficacy. Mechanistically, MCPIP1 does not
      affect the activation of JAK/STAT upstream of IFN-I signaling, but significantly 
      promotes IFN-I signaling by enhancing ISRE promoter activity and expression of
      interferon-stimulated genes (ISGs). And MCPIP1-mediated activation of IFN-I
      signaling is independently of its RNase and deubiquitinase activity. These
      findings uncover a novel innate antiviral mechanism mediated by the IFN-MCPIP1
      axis, and may provide potential targets for enhancing IFNs antiviral therapy.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Qian, Liping
AU  - Qian L
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Zuo, Yibo
AU  - Zuo Y
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Deng, Wenjun
AU  - Deng W
AD  - Department of Intensive Care Medicine, The First Affiliated Hospital of Soochow
      University, Suzhou, Jiangsu Province, 215123, China.
FAU - Miao, Ying
AU  - Miao Y
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Liu, Jin
AU  - Liu J
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Yuan, Yukang
AU  - Yuan Y
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Guo, Tingting
AU  - Guo T
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Zhang, Liting
AU  - Zhang L
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China.
FAU - Jin, Jun
AU  - Jin J
AD  - Department of Intensive Care Medicine, The First Affiliated Hospital of Soochow
      University, Suzhou, Jiangsu Province, 215123, China.
FAU - Wang, Jun
AU  - Wang J
AD  - Department of Intensive Care Medicine, The First Affiliated Hospital of Soochow
      University, Suzhou, Jiangsu Province, 215123, China. Electronic address:
      [email protected]
FAU - Zheng, Hui
AU  - Zheng H
AD  - Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu
      Province, 215123, China; Jiangsu Key Laboratory of Infection and Immunity,
      Soochow University, Suzhou, Jiangsu Province, 215123, China. Electronic address: 
      [email protected]
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180317
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Interferon Type I)
RN  - 0 (Transcription Factors)
RN  - EC 3.1.- (Ribonucleases)
RN  - EC 3.1.- (ZC3H12A protein, human)
SB  - IM
MH  - Cell Line
MH  - Humans
MH  - *Immunity, Innate
MH  - Interferon Type I/genetics/*immunology
MH  - Promoter Regions, Genetic
MH  - Response Elements/genetics
MH  - Ribonucleases/*immunology
MH  - Signal Transduction/immunology
MH  - Transcription Factors/*immunology
MH  - Transcriptional Activation
MH  - Transfection
MH  - Vesicular Stomatitis/immunology
MH  - Vesiculovirus/immunology
MH  - Virus Diseases/*immunology
OTO - NOTNLM
OT  - *Antiviral activity
OT  - *ISGs
OT  - *ISRE
OT  - *Interferon
OT  - *MCPIP1
EDAT- 2018/03/17 06:00
MHDA- 2018/04/14 06:00
CRDT- 2018/03/17 06:00
PHST- 2018/03/07 00:00 [received]
PHST- 2018/03/09 00:00 [accepted]
PHST- 2018/03/17 06:00 [pubmed]
PHST- 2018/04/14 06:00 [medline]
PHST- 2018/03/17 06:00 [entrez]
AID - S0006-291X(18)30562-X [pii]
AID - 10.1016/j.bbrc.2018.03.076 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Apr 15;498(4):891-897. doi:
      10.1016/j.bbrc.2018.03.076. Epub 2018 Mar 17.