Therapeutic Approaches to Type I Interferonopathies
Purpose of Review To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies. Summary Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activ...
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Published in | Current rheumatology reports Vol. 20; no. 6; p. 32 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Springer US
01.06.2018
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Subjects | |
Online Access | Get full text |
ISSN | 1523-3774 1534-6307 1534-6307 |
DOI | 10.1007/s11926-018-0743-3 |
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Abstract | Purpose of Review
To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies.
Summary
Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activation of antiviral type I interferon (IFN). Clinically, type I interferonopathies are characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic nucleic acid sensors. The type I IFN system is subject to a tight and complex regulation. Disturbances of its checks and balances can spark an unwanted immune response causing uncontrolled type I IFN signaling. Novel mechanistic insight into pathways that control the type I IFN system is providing opportunities for targeted therapeutic approaches by repurposing drugs such as Janus kinase inhibitors or reverse transcriptase inhibitors. |
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AbstractList | To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies. Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activation of antiviral type I interferon (IFN). Clinically, type I interferonopathies are characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic nucleic acid sensors. The type I IFN system is subject to a tight and complex regulation. Disturbances of its checks and balances can spark an unwanted immune response causing uncontrolled type I IFN signaling. Novel mechanistic insight into pathways that control the type I IFN system is providing opportunities for targeted therapeutic approaches by repurposing drugs such as Janus kinase inhibitors or reverse transcriptase inhibitors.PURPOSE OF REVIEWTo review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies. Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activation of antiviral type I interferon (IFN). Clinically, type I interferonopathies are characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic nucleic acid sensors. The type I IFN system is subject to a tight and complex regulation. Disturbances of its checks and balances can spark an unwanted immune response causing uncontrolled type I IFN signaling. Novel mechanistic insight into pathways that control the type I IFN system is providing opportunities for targeted therapeutic approaches by repurposing drugs such as Janus kinase inhibitors or reverse transcriptase inhibitors. To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies. Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activation of antiviral type I interferon (IFN). Clinically, type I interferonopathies are characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic nucleic acid sensors. The type I IFN system is subject to a tight and complex regulation. Disturbances of its checks and balances can spark an unwanted immune response causing uncontrolled type I IFN signaling. Novel mechanistic insight into pathways that control the type I IFN system is providing opportunities for targeted therapeutic approaches by repurposing drugs such as Janus kinase inhibitors or reverse transcriptase inhibitors. Purpose of Review To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies. Summary Type I interferonopathies represent a genetically and phenotypically heterogenous group of disorders of the innate immune system caused by constitutive activation of antiviral type I interferon (IFN). Clinically, type I interferonopathies are characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic nucleic acid sensors. The type I IFN system is subject to a tight and complex regulation. Disturbances of its checks and balances can spark an unwanted immune response causing uncontrolled type I IFN signaling. Novel mechanistic insight into pathways that control the type I IFN system is providing opportunities for targeted therapeutic approaches by repurposing drugs such as Janus kinase inhibitors or reverse transcriptase inhibitors. |
ArticleNumber | 32 |
Author | Griep, Constanze Lee-Kirsch, Min Ae Brück, Normi Wolf, Christine Tüngler, Victoria Kind, Barbara Berner, Reinhard Bienias, Marc Kretschmer, Stefanie |
Author_xml | – sequence: 1 givenname: Marc surname: Bienias fullname: Bienias, Marc organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 2 givenname: Normi surname: Brück fullname: Brück, Normi organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 3 givenname: Constanze surname: Griep fullname: Griep, Constanze organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 4 givenname: Christine surname: Wolf fullname: Wolf, Christine organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 5 givenname: Stefanie surname: Kretschmer fullname: Kretschmer, Stefanie organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 6 givenname: Barbara surname: Kind fullname: Kind, Barbara organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 7 givenname: Victoria surname: Tüngler fullname: Tüngler, Victoria organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 8 givenname: Reinhard surname: Berner fullname: Berner, Reinhard organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden – sequence: 9 givenname: Min Ae surname: Lee-Kirsch fullname: Lee-Kirsch, Min Ae email: minae.lee-kirsch@uniklinikum-dresden.de organization: Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29679241$$D View this record in MEDLINE/PubMed |
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To review recent scientific advances and therapeutic approaches in the expanding field of type I interferonopathies.
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SubjectTerms | Medicine Medicine & Public Health Pediatric Rheumatology (S Ozen Rheumatology Section Editor Topical Collection on Pediatric Rheumatology |
Title | Therapeutic Approaches to Type I Interferonopathies |
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