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J Mol Med (Berl). 2016 Oct;94(10):1103-1110. Epub 2016 Apr 20.

Cause and consequences of the activated type I interferon system in SLE.

Author information

1
Department of Medical Sciences, Rheumatology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
2
Department of Medical Sciences, Rheumatology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden. lars.ronnblom@medsci.uu.se.

Abstract

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.

KEYWORDS:

Etiopathogenesis; Immune regulation; Plasmacytoid dendritic cells; Systemic lupus erythematosus; Type I interferon

PMID:
27094810
PMCID:
PMC5052287
DOI:
10.1007/s00109-016-1421-4
[Indexed for MEDLINE]
Free PMC Article

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