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10.1038/s41577-021-00633-9

http://scihub22266oqcxt.onion/10.1038/s41577-021-00633-9
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34671122!8527296!34671122
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suck abstract from ncbi

pmid34671122      Nat+Rev+Immunol 2022 ; 22 (8): 471-483
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  • The type I interferonopathies: 10 years on #MMPMID34671122
  • Crow YJ; Stetson DB
  • Nat Rev Immunol 2022[Aug]; 22 (8): 471-483 PMID34671122show ga
  • As brutally demonstrated by the COVID-19 pandemic, an effective immune system is essential for survival. Developed over evolutionary time, viral nucleic acid detection is a central pillar in the defensive armamentarium used to combat foreign microbial invasion. To ensure cellular homeostasis, such a strategy necessitates the efficient discrimination of pathogen-derived DNA and RNA from that of the host. In 2011, it was suggested that an upregulation of type I interferon signalling might serve as a defining feature of a novel set of Mendelian inborn errors of immunity, where antiviral sensors are triggered by host nucleic acids due to a failure of self versus non-self discrimination. These rare disorders have played a surprisingly significant role in informing our understanding of innate immunity and the relevance of type I interferon signalling for human health and disease. Here we consider what we have learned in this time, and how the field may develop in the future.
  • |*COVID-19[MESH]
  • |*Interferon Type I/genetics[MESH]
  • |*Nucleic Acids[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]


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