Interferon-induced guanylate-binding proteins in inflammasome activation and host defense
In this Perspective, MacMicking and colleagues discuss the roles of interferon-induced guanylate-binding proteins in directing inflammasome responses and their effects on immunity to a wide variety of microbial pathogens. Traditional views of the inflammasome highlight the assembly of pre-existing c...
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| Published in | Nature immunology Vol. 17; no. 5; pp. 481 - 489 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.05.2016
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1529-2908 1529-2916 1529-2916 |
| DOI | 10.1038/ni.3440 |
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| Abstract | In this Perspective, MacMicking and colleagues discuss the roles of interferon-induced guanylate-binding proteins in directing inflammasome responses and their effects on immunity to a wide variety of microbial pathogens.
Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype–specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases. |
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| AbstractList | Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype-specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases. In this Perspective, MacMicking and colleagues discuss the roles of interferon-induced guanylate-binding proteins in directing inflammasome responses and their effects on immunity to a wide variety of microbial pathogens. Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype–specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases. Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype-specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases.Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype-specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases. |
| Audience | Academic |
| Author | Park, Eui-Soon Chee, Jonathan D Kim, Bae-Hoon Bradfield, Clinton J Kumar, Pradeep MacMicking, John D |
| Author_xml | – sequence: 1 givenname: Bae-Hoon surname: Kim fullname: Kim, Bae-Hoon organization: Howard Hughes Medical Institute, Yale University School of Medicine, Department of Microbial Pathogenesis, Yale University School of Medicine – sequence: 2 givenname: Jonathan D surname: Chee fullname: Chee, Jonathan D organization: Department of Microbial Pathogenesis, Yale University School of Medicine – sequence: 3 givenname: Clinton J surname: Bradfield fullname: Bradfield, Clinton J organization: Department of Microbial Pathogenesis, Yale University School of Medicine – sequence: 4 givenname: Eui-Soon surname: Park fullname: Park, Eui-Soon organization: Department of Microbial Pathogenesis, Yale University School of Medicine – sequence: 5 givenname: Pradeep surname: Kumar fullname: Kumar, Pradeep organization: Department of Microbial Pathogenesis, Yale University School of Medicine – sequence: 6 givenname: John D surname: MacMicking fullname: MacMicking, John D email: john.macmicking@yale.edu organization: Howard Hughes Medical Institute, Yale University School of Medicine, Department of Microbial Pathogenesis, Yale University School of Medicine, Department of Immunobiology, Yale University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27092805$$D View this record in MEDLINE/PubMed |
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| Snippet | In this Perspective, MacMicking and colleagues discuss the roles of interferon-induced guanylate-binding proteins in directing inflammasome responses and their... Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however,... |
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| SubjectTerms | 631/250/127/1212 631/250/2499 631/250/256/2177 Animals Binding proteins Biomedicine Disease Resistance - genetics Disease Resistance - immunology Genetic aspects GTP-Binding Proteins - classification GTP-Binding Proteins - genetics GTP-Binding Proteins - immunology Host-Pathogen Interactions - immunology Humans Immune response Immunology Infection - immunology Infection - microbiology Infection - parasitology Infectious Diseases Inflammasomes - genetics Inflammasomes - immunology Inflammasomes - metabolism Interferons - immunology Interferons - metabolism Listeria monocytogenes - immunology Listeria monocytogenes - physiology Mice Models, Immunological perspective Phylogeny Properties Signal Transduction - genetics Signal Transduction - immunology Toxoplasma - immunology Toxoplasma - physiology |
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| Title | Interferon-induced guanylate-binding proteins in inflammasome activation and host defense |
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