Interferon-Stimulated Genes: A Complex Web of Host Defenses

By W. Schneider, M. Chevillotte, Charles M. Rice. Annual Review of Immunology, 2014

2,878 citations recorded by the source corpus.

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.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/f50a6efddd9532a5b8c2cf795df6c2da6963642a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. G. Shadel
2. Aviv Regev
3. Tadatsugu Taniguchi
4. Nima Rezaei
5. D. Mathis
6. A. Misharin
7. Melika Lotfi
8. Tuo Li

In Oncology

1. Tadatsugu Taniguchi
2. Nima Rezaei
3. Melika Lotfi
4. Joachim L. Schultze
5. Stephen R. Quake
6. Michael R Hamblin

Citations in the corpus

• Coronavirus infections and immune responses (2020, background): “RIG‐I/NF‐κB‐dependent pathway(45) and the disorder of the JAK‐ STAT signaling pathway directly affects the spread of virus.(46) Although SARS‐CoV and other coronaviruses are sensitive to IFN‐a/b, these viruses remain highly pathogenic.”
• Parsing the interferon transcriptional network and its disease associations (2016, positive): “IFN induces a set of ‘‘interferon signature genes’’ (ISGs) that elicit a range of antiviral effectors (Schneider et al., 2014).”
• Evasion of Type I Interferon by SARS-CoV-2 (2020, background): “ISGF3 translocates to the nucleus and binds to IFN-Istimulated response elements (ISREs), triggering the expression of hundreds of ISGs with antiviral functions (Schneider et al., 2014; Schoggins et al., 2015).”
• Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions (2020, neutral): “As stated above, type-I IFN is critical for protecting against viral infections, since it promotes intracellular RNA degradation and virus clearance, induces tissue repair, and triggers a prolonged adaptive immune response [44] [45] [46] .”
• Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, background): “This signal induces the expression of hundreds of interferon-stimulated genes (ISGs) in the responding cell (Schneider et al., 2014).”
• COVID-19: Transmission, prevention, and potential therapeutic opportunities (2020, positive): “Interferons regulate the innate immune system, which is vital for killing viruses by regulating gene transcription [126].”
• SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues (2020, positive): “Canonical ISGs function by directly restricting viruses and reducing burden (Schneider et al., 2014).”