Journal
BEST PRACTICE & RESEARCH IN CLINICAL RHEUMATOLOGY
Volume 31, Issue 3, Pages 415-428Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.berh.2017.10.003
Keywords
Lupus erythematosus, systemic; Interferon type I; Plasmacytoid dendritic cell; Biologic therapy
Categories
Funding
- Swedish Research Council [A0258801]
- Swedish Rheumatism Foundation [R-662561]
- King Gustaf V's 80-Year Foundation [FAI-2015-0133]
- Knut and Alice Wallenberg Foundation [2011.0073]
- Alfred Osterlund's Foundation
- Anna-Greta Crafoord Foundation [20152011]
- Greta and Johan Kock's Fondation
- Medical Faculty of Lund University [436121]
- AstraZeneca Science for Life Laboratory research collaboration grant
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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects many different organ systems, with excessive production of type I interferons (IFNs) and auto antibodies against nucleic acids as hallmarks. Activation of the type I IFN system in SLE is due to continuous stimulation of plasmacytoid dendritic cells by endogenous nucleic acids, leading to sustained type I IFN production. This is reflected by an over expression of type I IFN-regulated genes or an IFN signature. Type I IFNs have effects on both the innate and adaptive immune systems, which contribute to both loss of tolerance and the autoimmune disease process. In this review, we discuss the current understanding of IFNs in SLE, focusing on their regulation, the influence of genetic background, and environmental factors and therapies that are under development aiming to inhibit the type I IFN system in SLE. (C) 2017 Elsevier Ltd. All rights reserved.
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