期刊
JOURNAL OF MOLECULAR MEDICINE-JMM
卷 94, 期 10, 页码 1103-1110出版社
SPRINGER
DOI: 10.1007/s00109-016-1421-4
关键词
Type I interferon; Systemic lupus erythematosus; Plasmacytoid dendritic cells; Etiopathogenesis; Immune regulation
资金
- Swedish Research Council are the Swedish Rheumatism Foundation
- King Gustaf V's 80-Year Foundation
- Knut and Alice Wallenberg Foundation
- AstraZeneca Science for Life Laboratory
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.
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