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10.1084/jem.20140995 http://scihub22266oqcxt.onion/10.1084/jem.20140995 C4451128!4451128 !25941255     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25941255 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Exp+Med 2015 ; 212 (6 ): 845-53 Nephropedia Template TP {{tp|p=25941255 |t=2015. IFN-? resolves inflammation via suppression of neutrophil infiltration and IL-1? production |pdf=|usr=}}{{25941255 }} gab.com Text IFN- resolves inflammation via suppression of neutrophil infiltration and IL-1 production JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=25941255 #FOAvip The most studied biological role of type III interferons (IFNs) has so far been their antiviral activity, but their role in autoimmune and inflammatory diseases remains largely unexplored. Here, we show that treatment with IFN-?2/IL-28A completely halts and reverses the development of collagen-induced arthritis (CIA) and discover cellular and molecular mechanisms of IL-28A antiinflammatory function. We demonstrate that treatment with IL-28A dramatically reduces numbers of proinflammatory IL-17-producing Th17 and ?? T cells in the joints and inguinal lymph nodes, without affecting T cell proliferative responses or levels of anticollagen antibodies. IL-28A exerts its antiinflammatory effect by restricting recruitment of IL-1b-expressing neutrophils, which are important for amplification of inflammation. We identify neutrophils as cells expressing high levels of IFN-? receptor 1 (IFNLR1)-IL-28 receptor ? (IL28RA) and targeted by IL-28A. Our data highlight neutrophils as contributors to the pathogenesis of autoimmune arthritis and present IFN-?s or agonists of IFNLR1-IL28RA as putative new therapeutics for neutrophil-driven inflammation. Twit Text FOAVip IFN- resolves inflammation via suppression of neutrophil infiltration and IL-1 production ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=25941255 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25941255 #FOAvip English Wikipedia <ref>{{Cite pmid|25941255 }}</ref> IFN-? resolves inflammation via suppression of neutrophil infiltration and IL-1? production #MMPMID25941255 Blazek K ; Eames HL ; Weiss M ; Byrne AJ ; Perocheau D ; Pease JE ; Doyle S ; McCann F ; Williams RO ; Udalova IA J Exp Med 2015[Jun]; 212 (6 ): 845-53 PMID25941255 show ga The most studied biological role of type III interferons (IFNs) has so far been their antiviral activity, but their role in autoimmune and inflammatory diseases remains largely unexplored. Here, we show that treatment with IFN-?2/IL-28A completely halts and reverses the development of collagen-induced arthritis (CIA) and discover cellular and molecular mechanisms of IL-28A antiinflammatory function. We demonstrate that treatment with IL-28A dramatically reduces numbers of proinflammatory IL-17-producing Th17 and ?? T cells in the joints and inguinal lymph nodes, without affecting T cell proliferative responses or levels of anticollagen antibodies. IL-28A exerts its antiinflammatory effect by restricting recruitment of IL-1b-expressing neutrophils, which are important for amplification of inflammation. We identify neutrophils as cells expressing high levels of IFN-? receptor 1 (IFNLR1)-IL-28 receptor ? (IL28RA) and targeted by IL-28A. Our data highlight neutrophils as contributors to the pathogenesis of autoimmune arthritis and present IFN-?s or agonists of IFNLR1-IL28RA as putative new therapeutics for neutrophil-driven inflammation. |*Gene Expression Regulation [MESH] |Animals [MESH] |Arthritis/metabolism [MESH] |CD4-Positive T-Lymphocytes/cytology [MESH] |Cattle [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Chickens [MESH] |Collagen/chemistry [MESH] |Flow Cytometry [MESH] |Inflammation/*metabolism [MESH] |Interleukin-17/metabolism [MESH] |Interleukin-1beta/*metabolism [MESH] |Interleukins/*pharmacology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Inbred DBA [MESH] |Neutrophils/cytology/metabolism [MESH] |Receptors, Antigen, T-Cell, gamma-delta/metabolism [MESH] |Receptors, Cytokine/metabolism [MESH]IFN-? resolves inflammation via suppression of neutrophil infiltration(epmc).pdf DeepDyve Pubget Overpricing