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10.1007/s00109-016-1421-4 http://scihub22266oqcxt.onion/10.1007/s00109-016-1421-4 27094810!5052287!27094810     free     free     free       J+Mol+Med+(Berl) 2016 ; 94 (10): 1103-1110 Nephropedia Template TP {{tp|p=27094810|t=2016. Cause and consequences of the activated type I interferon system in SLE |pdf=|usr=}}{{27094810}} gab.com Text Cause and consequences of the activated type I interferon system in SLE JO: J Mol Med (Berl) http://www.kidney.de/pget.php?&tw=1&pmid=27094810 #FOAvip 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. Twit Text FOAVip Cause and consequences of the activated type I interferon system in SLE ????J Mol Med (Berl) http://www.kidney.de/pget.php?&tw=1&pmid=27094810 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27094810 #FOAvip English Wikipedia <ref>{{Cite pmid|27094810}}</ref> Cause and consequences of the activated type I interferon system in SLE #MMPMID27094810 Eloranta ML; Ronnblom L J Mol Med (Berl) 2016[Oct]; 94 (10): 1103-1110 PMID27094810show ga 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. |Interferon Type I/antagonists & inhibitors/*immunology[MESH] |Lupus Erythematosus, Systemic/drug therapy/genetics/*immunology[MESH]Cause and consequences of the activated type I interferon system in SL(epmc).pdf DeepDyve Pubget Overpricing