Mouse models of type I interferonopathies
Mouse models of type I interferonopathies
View/Date of Publication
16.12.2024Publisher
Oxford University PressPublisher Location
OxfordMetadata
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Citable Link (Handle URI) 
https://hdl.handle.net/20.500.11811/13361
Abstract
Type I interferonopathies are severe monogenic diseases caused by mutations that result in chronically upregulated production of type I interferon. They present with a broad variety of symptoms, the mechanisms of which are being extensively studied. Mouse models of type I interferonopathies are an important resource for this purpose, and in this context, we review several key molecular and phenotypic findings that are advancing our understanding of the respective diseases. We focus on genotypes related to nucleic acid metabolism, sensing by cytosolic receptors and downstream signalling.
Subjects
Innate immunity, Innate sensors, Type I interferon, Autoimmunity
Classification (DDC)
570 Biowissenschaften, Biologie 610 Medizin, GesundheitPublished in
Human Molecular Genetics, 2024, ddae187, pp. 1-9First Publication
https://doi.org/10.1093/hmg/ddae187Luca, Domnica; Kato, Hiroki: Mouse models of type I interferonopathies. In: Human Molecular Genetics. 2024, ddae187, 1-9.
Online-Ausgabe in bonndoc: https://hdl.handle.net/20.500.11811/13361
Online-Ausgabe in bonndoc: https://hdl.handle.net/20.500.11811/13361
@article{handle:20.500.11811/13361,
author = {{Domnica Luca} and {Hiroki Kato}},
title = {Mouse models of type I interferonopathies},
publisher = {Oxford University Press},
year = 2024,
month = dec,
journal = {Human Molecular Genetics},
volume = 2024, ddae187,
pages = 1--9,
note = {Type I interferonopathies are severe monogenic diseases caused by mutations that result in chronically upregulated production of type I interferon. They present with a broad variety of symptoms, the mechanisms of which are being extensively studied. Mouse models of type I interferonopathies are an important resource for this purpose, and in this context, we review several key molecular and phenotypic findings that are advancing our understanding of the respective diseases. We focus on genotypes related to nucleic acid metabolism, sensing by cytosolic receptors and downstream signalling.},
url = {https://hdl.handle.net/20.500.11811/13361}
}
author = {{Domnica Luca} and {Hiroki Kato}},
title = {Mouse models of type I interferonopathies},
publisher = {Oxford University Press},
year = 2024,
month = dec,
journal = {Human Molecular Genetics},
volume = 2024, ddae187,
pages = 1--9,
note = {Type I interferonopathies are severe monogenic diseases caused by mutations that result in chronically upregulated production of type I interferon. They present with a broad variety of symptoms, the mechanisms of which are being extensively studied. Mouse models of type I interferonopathies are an important resource for this purpose, and in this context, we review several key molecular and phenotypic findings that are advancing our understanding of the respective diseases. We focus on genotypes related to nucleic acid metabolism, sensing by cytosolic receptors and downstream signalling.},
url = {https://hdl.handle.net/20.500.11811/13361}
}
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