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Endogenous type I interferon inducers in autoimmune diseases
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. (Systemic Autoimmunity)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. (Systemic Autoimmunity)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. (Systemic Autoimmunity)
2009 (English)In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 42, no 4, 349-352 p.Article, review/survey (Refereed) Published
Abstract [en]

Type I interferon (IFN) is produced by the innate immune system in several autoimmune diseases, such as systemic lupus erythematosus (SLE), polymyositis, and systemic sclerosis. In these diseases, immune complex (IC)-containing DNA or RNA may act as endogenous IFN inducers. The abilities of these IC to reach the endosomes in the plasmacytoid dendritic cells (PDC) cause the intracellular toll-like receptor (TLR) to initiate a cascade of transcription factors--a critical step in triggering type I IFN production. A special configuration of the nucleic acid (NA), such as CpG-rich non-methylated DNA or GU-rich RNA, appears crucial. However, other components of the IC, like HMGB1, may also be necessary. Studies regarding the genetic background of autoimmune diseases suggest that variants of genes involved in both IFN production and response are associated with disease susceptibility. This knowledge is important for the development of new therapeutic strategies in autoimmune diseases.

Place, publisher, year, edition, pages
2009. Vol. 42, no 4, 349-352 p.
Keyword [en]
type I IFN, interferon, lupus, SLE
National Category
Medical and Health Sciences
Research subject
Medicine
Identifiers
URN: urn:nbn:se:uu:diva-110974DOI: 10.1080/08916930902831829ISI: 000268967900034PubMedID: 19811298OAI: oai:DiVA.org:uu-110974DiVA: diva2:304745
Available from: 2010-03-19 Created: 2009-12-01 Last updated: 2017-12-12Bibliographically approved

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Eloranta, Maija-LeenaRönnblom, Lars

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