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10.3390/ijms21239249 http://scihub22266oqcxt.onion/10.3390/ijms21239249 33291536!7730283!33291536     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Sci 2020 ; 21 (23): ä Nephropedia Template TP {{tp|p=33291536|t=2020. The STING-IFN-beta-Dependent Axis Is Markedly Low in Patients with Relapsing-Remitting Multiple Sclerosis |pdf=|usr=}}{{33291536}} gab.com Text The STING-IFN-beta-Dependent Axis Is Markedly Low in Patients with Relapsing-Remitting Multiple Sclerosis JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33291536 #FOAvip Cyclic GMP-AMP-synthase is a sensor of endogenous nucleic acids, which subsequently elicits a stimulator of interferon genes (STING)-dependent type I interferon (IFN) response defending us against viruses and other intracellular pathogens. This pathway can drive pathological inflammation, as documented for type I interferonopathies. In contrast, specific STING activation and subsequent IFN-beta release have shown beneficial effects on experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). Although less severe cases of relapse-remitting MS (RRMS) are treated with IFN-beta, there is little information correlating aberrant type I IFN signaling and the pathologic conditions of MS. We hypothesized that there is a link between STING activation and the endogenous production of IFN-beta during neuroinflammation. Gene expression analysis in EAE mice showed that Sting level decreased in the peripheral lymphoid tissue, while its level increased within the central nervous system over the course of the disease. Similar patterns could be verified in peripheral immune cells during the acute phases of RRMS in comparison to remitting phases and appropriately matched healthy controls. Our study is the first to provide evidence that the STING/IFN-beta-axis is downregulated in RRMS patients, meriting further intensified research to understand its role in the pathophysiology of MS and potential translational applications. Twit Text FOAVip The STING-IFN-beta-Dependent Axis Is Markedly Low in Patients with Relapsing-Remitting Multiple Sclerosis ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33291536 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33291536 #FOAvip English Wikipedia <ref>{{Cite pmid|33291536}}</ref> The STING-IFN-beta-Dependent Axis Is Markedly Low in Patients with Relapsing-Remitting Multiple Sclerosis #MMPMID33291536 Masanneck L; Eichler S; Vogelsang A; Korsen M; Wiendl H; Budde T; Meuth SG Int J Mol Sci 2020[Dec]; 21 (23): ä PMID33291536show ga Cyclic GMP-AMP-synthase is a sensor of endogenous nucleic acids, which subsequently elicits a stimulator of interferon genes (STING)-dependent type I interferon (IFN) response defending us against viruses and other intracellular pathogens. This pathway can drive pathological inflammation, as documented for type I interferonopathies. In contrast, specific STING activation and subsequent IFN-beta release have shown beneficial effects on experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). Although less severe cases of relapse-remitting MS (RRMS) are treated with IFN-beta, there is little information correlating aberrant type I IFN signaling and the pathologic conditions of MS. We hypothesized that there is a link between STING activation and the endogenous production of IFN-beta during neuroinflammation. Gene expression analysis in EAE mice showed that Sting level decreased in the peripheral lymphoid tissue, while its level increased within the central nervous system over the course of the disease. Similar patterns could be verified in peripheral immune cells during the acute phases of RRMS in comparison to remitting phases and appropriately matched healthy controls. Our study is the first to provide evidence that the STING/IFN-beta-axis is downregulated in RRMS patients, meriting further intensified research to understand its role in the pathophysiology of MS and potential translational applications. |*Signal Transduction[MESH] |Biomarkers[MESH] |Central Nervous System/metabolism/pathology[MESH] |Disease Susceptibility[MESH] |Flow Cytometry[MESH] |Gene Expression[MESH] |Humans[MESH] |Interferon-beta/*metabolism[MESH] |Leukocytes, Mononuclear/immunology/metabolism[MESH] |Membrane Proteins/genetics/*metabolism[MESH] |Multiple Sclerosis, Relapsing-Remitting/etiology/*metabolism[MESH]The STING-IFN-beta-Dependent Axis Is Markedly Low in Patients with Re(epmc).pdf DeepDyve Pubget Overpricing