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- W2338592803 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." @default.
- W2338592803 created "2016-06-24" @default.
- W2338592803 creator A5055854855 @default.
- W2338592803 creator A5078557164 @default.
- W2338592803 date "2016-04-20" @default.
- W2338592803 modified "2023-10-17" @default.
- W2338592803 title "Cause and consequences of the activated type I interferon system in SLE" @default.
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- W2338592803 doi "https://doi.org/10.1007/s00109-016-1421-4" @default.
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