Cause and consequences of the activated type I interferon system in SLE.
2016 (English)In: Journal of Molecular Medicine, ISSN 0946-2716, E-ISSN 1432-1440Article in journal (Refereed) Epub ahead of print
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
Rheumatology and Autoimmunity Rheumatology and Autoimmunity
Research subject Medical Science
IdentifiersURN: urn:nbn:se:uu:diva-300370DOI: 10.1007/s00109-016-1421-4PubMedID: 27094810OAI: oai:DiVA.org:uu-300370DiVA: diva2:951345