Interferon-Stimulated Genes: A Complex Web of Host Defenses

被引：2247

作者：

Schneider, William M. ^{[1
]}

Chevillotte, Meike Dittmann ^{[1
]}

Rice, Charles M. ^{[1
]}

机构：

[1] Rockefeller Univ, Lab Virol & Infect Dis, New York, NY 10065 USA

来源：

ANNUAL REVIEW OF IMMUNOLOGY, VOL 32 | 2014年 / 32卷

关键词：

innate immunity; pathogen recognition; desensitization; antiviral effectors; CYCLIC GMP-AMP; C VIRUS-REPLICATION; WEST NILE VIRUS; PROTEIN-TYROSINE-PHOSPHATASE; TRIM FAMILY PROTEINS; E3 UBIQUITIN LIGASE; JAK-STAT PATHWAY; ANTIVIRAL ACTIVITY; TRANSCRIPTION FACTOR; SIGNAL-TRANSDUCTION;

D O I：

10.1146/annurev-immunol-032713-120231

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Interferon-stimulated gene (ISG) products take on a number of diverse roles. Collectively, they are highly effective at resisting and controlling pathogens. In this review, we begin by introducing interferon (IFN) and the JAK-STAT signaling pathway to highlight features that impact ISG production. Next, we describe ways in which ISGs both enhance innate pathogen-sensing capabilities and negatively regulate signaling through the JAK-STAT pathway. Several ISGs that directly inhibit virus infection are described with an emphasis on those that impact early and late stages of the virus life cycle. Finally, we describe ongoing efforts to identify and characterize antiviral ISGs, and we provide a forward-looking perspective on the ISG landscape.

引用

页码：513 / 545

页数：33

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