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The interferon signature in autoimmune diseases
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology.
2013 (English)In: Current Opinion in Rheumatology, ISSN 1040-8711, E-ISSN 1531-6963, Vol. 25, no 2, 248-253 p.Article, review/survey (Refereed) Published
Abstract [en]

PURPOSE OF REVIEW:

An increased expression of type I interferon (IFN) regulated genes (an IFN signature) has been reported in blood and tissue cells from patients with SLE and other autoimmune diseases. We review the possible mechanisms behind the IFN signature as well as clinical and therapeutic consequences of this observation.

RECENT FINDINGS:

Autoantigens from dying cells trigger plasmacytoid dendritic cells to a continuous synthesis of type I IFN, which is promoted by natural killer (NK) cells and B cells. A growing number of genes connected to type I IFN production and response associates with an increased susceptibility to autoimmunity. Besides type I IFN, type III IFN (IFN-λ) may contribute to the IFN signature. In SLE and primary Sjögren's syndrome, a prominent IFN signature is connected to an active disease, whereas in rheumatoid arthritis the IFN signature defines a disease subset with poor clinical outcome and treatment failure to B-cell depleting therapy. Several therapies aiming to inhibit the IFN signature are in clinical trials and early data suggest clinical benefits without major safety problems.

SUMMARY:

The observed IFN signature in several autoimmune diseases is a biomarker of active disease and is investigated as a tool when selecting treatment for individual patients.

Place, publisher, year, edition, pages
2013. Vol. 25, no 2, 248-253 p.
Keyword [en]
SLE, interferon
National Category
Rheumatology and Autoimmunity
Identifiers
URN: urn:nbn:se:uu:diva-190942DOI: 10.1097/BOR.0b013e32835c7e32ISI: 000314398600015PubMedID: 23249830OAI: oai:DiVA.org:uu-190942DiVA: diva2:584535
Available from: 2013-01-09 Created: 2013-01-09 Last updated: 2017-12-06Bibliographically approved

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Rönnblom, LarsEloranta, Maija-Leena

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