title: Type I interferons: crucial participants in disease amplification in autoimmunity.
abstract: A significant body of data implicates the type I interferon (IFN) pathway in the pathogenesis of autoimmune rheumatic diseases. In these disorders, a self-reinforcing cycle of IFN production can contribute to immunopathology through multiple mechanisms. Type I IFN cytokines are pleiotropic in their effects, mediating antiviral and antitumor activities, and possess numerous immunomodulatory functions for both the innate and adaptive immune responses. A key principle of the type I IFN system is rapid induction and amplification of the signaling pathway, which generates a feed-forward loop of IFN production, ensuring that a vigorous antiviral immune response is mounted. Although such feed-forward pathways are highly adaptive when it comes to rapid and effective virus eradication, this amplification can be maladaptive in immune responses directed against host tissues. Such feed-forward loops, however, create special opportunities for therapy.
authors.affiliation: Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, 5200 Eastern Avenue, Mason F. Lord Building, Center Tower, Suite 4100, Room 412, Baltimore, MD 21224, USA.
authors.forename: John C
authors.initials: JC
authors.lastname: Hall
authors.forename: Antony
authors.initials: A
authors.lastname: Rosen
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000378:metabolism*; D006801:Humans; D007370:Interferon Type I / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D007370:Interferon Type I