物候学
Ⅰ型干扰素
免疫
生物
自身免疫
干扰素
炎症
呼吸系统
免疫学
免疫系统
表型
基因
遗传学
解剖
作者
Yanick J. Crow,Jean‐Laurent Casanova
出处
期刊:Science immunology
[American Association for the Advancement of Science (AAAS)]
日期:2024-07-05
卷期号:9 (97)
标识
DOI:10.1126/sciimmunol.adm8185
摘要
The past 20 years have seen the definition of human monogenic disorders and their autoimmune phenocopies underlying either defective or enhanced type I interferon (IFN) activity. These disorders delineate the impact of type I IFNs in natural conditions and demonstrate that only a narrow window of type I IFN activity is beneficial. Insufficient type I IFN predisposes humans to life-threatening viral diseases (albeit unexpectedly few) with a central role in immunity to respiratory and cerebral viral infection. Excessive type I IFN, perhaps counterintuitively, appears to underlie a greater number of autoinflammatory and/or autoimmune conditions known as type I interferonopathies, whose study has revealed multiple molecular programs involved in the induction of type I IFN signaling. These observations suggest that the manipulation of type I IFN activity to within a physiological range may be clinically relevant for the prevention and treatment of viral and inflammatory diseases.
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