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Systemic lupus erythematosus: a disease with a dysregulated type I interferon system
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology. Uppsala University, Science for Life Laboratory, SciLifeLab.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology. Uppsala University, Science for Life Laboratory, SciLifeLab.
2015 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 82, no 3, 199-207 p.Article, review/survey (Refereed) Published
Abstract [en]

Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease characterized by the loss of tolerance to nuclear antigens, immune complex formation and inflammation in multiple organs. The disease is very heterogeneous and most clinicians consider SLE as a group of diseases with similar features where the pathogenesis is driven by a combination of genetic and environmental factors. One of the most prominent features, shared by the majority of SLE patients, is a continuous activation of the type I interferon (IFN) system, which manifests as increased serum levels of IFNα and/or an increased expression of type I IFN induced genes, a so called type I IFN-signature. The mechanisms behind this IFN-signature have partly been clarified during recent years, although the exact function of the IFN regulated genes in the disease process is unclear. In this review we will describe the type I IFN system and its regulation and summarize the numerous findings implicating an important ethiopathogenic role of a dysregulated type I IFN system in SLE. Furthermore, strategies to therapeutically target the type I IFN system that are currently evaluated preclinically and in clinical trials will be mentioned.

Place, publisher, year, edition, pages
2015. Vol. 82, no 3, 199-207 p.
National Category
Rheumatology and Autoimmunity
Identifiers
URN: urn:nbn:se:uu:diva-259463DOI: 10.1111/sji.12330ISI: 000360044100006PubMedID: 26099519OAI: oai:DiVA.org:uu-259463DiVA: diva2:844271
Available from: 2015-08-04 Created: 2015-08-04 Last updated: 2017-12-04Bibliographically approved

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Hagberg, NiklasRönnblom, Lars

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