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10.1016/j.celrep.2020.108407 http://scihub22266oqcxt.onion/10.1016/j.celrep.2020.108407 33207208!7727402!33207208     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2020 ; 33 (7): 108407 Nephropedia Template TP {{tp|p=33207208|t=2020. JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome |pdf=|usr=}}{{33207208}} gab.com Text JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33207208 #FOAvip Individuals with Down syndrome (DS; trisomy 21) display hyperactivation of interferon (IFN) signaling and chronic inflammation, which could potentially be explained by the extra copy of four IFN receptor (IFNR) genes encoded on chromosome 21. However, the clinical effects of IFN hyperactivity in DS remain undefined. Here, we report that a commonly used mouse model of DS overexpresses IFNR genes and shows hypersensitivity to IFN ligands in diverse immune cell types. When treated repeatedly with a TLR3 agonist to induce chronic inflammation, these animals overexpress key IFN-stimulated genes, induce cytokine production, exhibit liver pathology, and undergo rapid weight loss. Importantly, the lethal immune hypersensitivity and cytokine production and the ensuing pathology are ameliorated by JAK1 inhibition. These results indicate that individuals with DS may experience harmful hyperinflammation upon IFN-inducing immune stimuli, as observed during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, pointing to JAK1 inhibition as a strategy to restore immune homeostasis in DS. Twit Text FOAVip JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33207208 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33207208 #FOAvip English Wikipedia <ref>{{Cite pmid|33207208}}</ref> JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome #MMPMID33207208 Tuttle KD; Waugh KA; Araya P; Minter R; Orlicky DJ; Ludwig M; Andrysik Z; Burchill MA; Tamburini BAJ; Sempeck C; Smith K; Granrath R; Tracy D; Baxter J; Espinosa JM; Sullivan KD Cell Rep 2020[Nov]; 33 (7): 108407 PMID33207208show ga Individuals with Down syndrome (DS; trisomy 21) display hyperactivation of interferon (IFN) signaling and chronic inflammation, which could potentially be explained by the extra copy of four IFN receptor (IFNR) genes encoded on chromosome 21. However, the clinical effects of IFN hyperactivity in DS remain undefined. Here, we report that a commonly used mouse model of DS overexpresses IFNR genes and shows hypersensitivity to IFN ligands in diverse immune cell types. When treated repeatedly with a TLR3 agonist to induce chronic inflammation, these animals overexpress key IFN-stimulated genes, induce cytokine production, exhibit liver pathology, and undergo rapid weight loss. Importantly, the lethal immune hypersensitivity and cytokine production and the ensuing pathology are ameliorated by JAK1 inhibition. These results indicate that individuals with DS may experience harmful hyperinflammation upon IFN-inducing immune stimuli, as observed during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, pointing to JAK1 inhibition as a strategy to restore immune homeostasis in DS. |Animals[MESH] |Azetidines/*therapeutic use[MESH] |Down Syndrome/complications/*immunology[MESH] |Female[MESH] |Hypersensitivity/*drug therapy/etiology/immunology[MESH] |Immunity, Innate[MESH] |Interferon-alpha/metabolism[MESH] |Janus Kinase 1/*antagonists & inhibitors[MESH] |Janus Kinase 2/*antagonists & inhibitors[MESH] |Liver/immunology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Protein Kinase Inhibitors/*therapeutic use[MESH] |Purines[MESH] |Pyrazoles[MESH] |Sulfonamides/*therapeutic use[MESH]JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model(epmc).pdf DeepDyve Pubget Overpricing