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Cause and consequences of the activated type I interferon system in SLE
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology. (Reumatologi)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology. (Reumatologi)
2016 (English)In: Journal of Molecular Medicine, ISSN 0946-2716, E-ISSN 1432-1440, Vol. 94, no 10, 1103-1110 p.Article in journal (Refereed) Published
Abstract [en]

Patients with systemic lupus erythematosus (SLE) have an increased expression of type I interferon (IFN)-regulated genes (an IFN signature), which is caused by an ongoing production of type I IFNs by plasmacytoid dendritic cells (pDCs). The reasons behind the continuous IFN production in SLE are the presence of self-derived IFN inducers and a lack of negative feed-back signals that downregulate the IFN response. In addition, several cells in the immune system promote the IFN production by pDCs and gene variants in the type I IFN signaling pathway contribute to the IFN signature. The type I IFNs act as an immune adjuvant and stimulate T cells, B cells, and monocytes, which all play an important role in the loss of tolerance and persistent autoimmune reaction in SLE. Consequently, new treatments aiming to inhibit the activated type I IFN system in SLE are now being developed and investigated in clinical trials.

Place, publisher, year, edition, pages
2016. Vol. 94, no 10, 1103-1110 p.
Keyword [en]
Type I interferon; Systemic lupus erythematosus; Plasmacytoid dendritic cells; Etiopathogenesis; Immune regulation
National Category
Rheumatology and Autoimmunity Rheumatology and Autoimmunity
Research subject
Medical Science
Identifiers
URN: urn:nbn:se:uu:diva-300370DOI: 10.1007/s00109-016-1421-4ISI: 000385250200004PubMedID: 27094810OAI: oai:DiVA.org:uu-300370DiVA: diva2:951345
Funder
Knut and Alice Wallenberg FoundationAstraZeneca
Available from: 2016-08-08 Created: 2016-08-08 Last updated: 2016-12-05Bibliographically approved

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