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Nat Rev Rheumatol. 2010 Jan;6(1):40-9. doi: 10.1038/nrrheum.2009.237.

Type I interferons: crucial participants in disease amplification in autoimmunity.

Author information

1
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.

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.

PMID:
20046205
PMCID:
PMC3622245
DOI:
10.1038/nrrheum.2009.237
[Indexed for MEDLINE]
Free PMC Article

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