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Autoantibodies targeting type I interferons: Prevalence, mechanisms of induction, and association with viral disease susceptibility
- Source :
- Hale, Benjamin G (2023). Autoantibodies targeting type I interferons: Prevalence, mechanisms of induction, and association with viral disease susceptibility. European Journal of Immunology, 53(6):e2250164.
- Publication Year :
- 2023
-
Abstract
- The type I IFN (IFN-I) system is essential to limit severe viral disease in humans. Thus, IFN-I deficiencies are associated with serious life-threatening infections. Remarkably, some rare individuals with chronic autoimmune diseases develop neutralizing autoantibodies (autoAbs) against IFN-Is thereby compromising their own innate antiviral defenses. Furthermore, the prevalence of anti-IFN-I autoAbs in apparently healthy individuals increases with age, such that ∼4% of those over 70 years old are affected. Here, I review the literature on factors that may predispose individuals to develop anti-IFN-I autoAbs, such as reduced self-tolerance caused by defects in the genes AIRE, NFKB2, and FOXP3 (among others), or by generally impaired thymus function, including thymic involution in the elderly. In addition, I discuss the hypothesis that predisposed individuals develop anti-IFN-I autoAbs following "autoimmunization" with IFN-Is generated during some acute viral infections, systemic inflammatory events, or chronic IFN-I exposure. Finally, I highlight the enhanced susceptibility that individuals with anti-IFN-I autoAbs appear to have towards viral diseases such as severe COVID-19, influenza, or herpes (e.g., varicella-zoster virus, herpes simplex virus, cytomegalovirus), as well as adverse reactions to live-attenuated vaccines. Understanding the mechanisms underlying development and consequences of anti-IFN-I autoAbs will be key to implementing effective prophylactic and therapeutic measures.
Details
- Database :
- OAIster
- Journal :
- Hale, Benjamin G (2023). Autoantibodies targeting type I interferons: Prevalence, mechanisms of induction, and association with viral disease susceptibility. European Journal of Immunology, 53(6):e2250164.
- Notes :
- application/pdf, info:doi/10.5167/uzh-252992, English, English
- Publication Type :
- Electronic Resource
- Accession number :
- edsoai.on1443056899
- Document Type :
- Electronic Resource