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10.1186/s13075-018-1560-9 http://scihub22266oqcxt.onion/10.1186/s13075-018-1560-9 C5887260!5887260!29622035     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arthritis+Res+Ther 2018 ; 20 (ä): ä Nephropedia Template TP {{tp|p=29622035|t=2018. CCL17 blockade as a therapy for osteoarthritis pain and disease |pdf=|usr=}}{{29622035}} gab.com Text CCL17 blockade as a therapy for osteoarthritis pain and disease JO: Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=29622035 #FOAvip Background: Granulocyte macrophage-colony stimulating factor (GM-CSF) has been implicated in the pathogenesis of a number of inflammatory diseases and in osteoarthritis (OA). We identified previously a new GM-CSF?Jmjd3?interferon regulatory factor 4 (IRF4)?chemokine (c-c motif) ligand 17 (CCL17) pathway, which is important for the development of inflammatory arthritis pain and disease. Tumour necrosis factor (TNF) can also be linked with this pathway. Here we investigated the involvement of the pathway in OA pain and disease development using the GM-CSF-dependent collagenase-induced OA (CiOA) model. Methods: CiOA was induced in C57BL/6 wild-type (WT), Irf4?/?, Ccl17E/E, Ccr4?/?, Tnf?/? and GM-CSF?/? mice. Additionally, therapeutic targeting of CCL17, Jmjd3 and cyclooxygenase 2 (COX-2) was evaluated. Development of pain (assessment of weight distribution) and OA disease (histologic scoring of synovitis, cartilage destruction and osteophyte size) were assessed. Synovial joint cells, including neutrophils, macrophages, fibroblasts and endothelial cells, were isolated (cell sorting) and gene expression analyzed (quantitative PCR). Results: Studies in the gene-deficient mice indicated that IRF4, CCL17 and the CCL17 receptor, CCR4, but not TNF, were required for CiOA pain and optimal cartilage destruction and osteophyte size. Therapeutic neutralization of CCL17 and Jmjd3 ameliorated both pain and disease, whereas the COX-2 inhibitor only ameliorated pain. In the synovium Ccl17 mRNA was expressed only in the macrophages in a GM-CSF-dependent and IRF4-dependent manner. Conclusions: The GM-CSF?Jmjd3?IRF4?CCL17 pathway is important for the development of CiOA, with CCL17 thus being a potential therapeutic target for the treatment of both OA pain and disease. Electronic supplementary material: The online version of this article (10.1186/s13075-018-1560-9) contains supplementary material, which is available to authorized users. Twit Text FOAVip CCL17 blockade as a therapy for osteoarthritis pain and disease ????Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=29622035 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29622035 #FOAvip English Wikipedia <ref>{{Cite pmid|29622035}}</ref> CCL17 blockade as a therapy for osteoarthritis pain and disease #MMPMID29622035 Lee MC; Saleh R; Achuthan A; Fleetwood AJ; Förster I; Hamilton JA; Cook AD Arthritis Res Ther 2018[]; 20 (ä): ä PMID29622035show ga Background: Granulocyte macrophage-colony stimulating factor (GM-CSF) has been implicated in the pathogenesis of a number of inflammatory diseases and in osteoarthritis (OA). We identified previously a new GM-CSF?Jmjd3?interferon regulatory factor 4 (IRF4)?chemokine (c-c motif) ligand 17 (CCL17) pathway, which is important for the development of inflammatory arthritis pain and disease. Tumour necrosis factor (TNF) can also be linked with this pathway. Here we investigated the involvement of the pathway in OA pain and disease development using the GM-CSF-dependent collagenase-induced OA (CiOA) model. Methods: CiOA was induced in C57BL/6 wild-type (WT), Irf4?/?, Ccl17E/E, Ccr4?/?, Tnf?/? and GM-CSF?/? mice. Additionally, therapeutic targeting of CCL17, Jmjd3 and cyclooxygenase 2 (COX-2) was evaluated. Development of pain (assessment of weight distribution) and OA disease (histologic scoring of synovitis, cartilage destruction and osteophyte size) were assessed. Synovial joint cells, including neutrophils, macrophages, fibroblasts and endothelial cells, were isolated (cell sorting) and gene expression analyzed (quantitative PCR). Results: Studies in the gene-deficient mice indicated that IRF4, CCL17 and the CCL17 receptor, CCR4, but not TNF, were required for CiOA pain and optimal cartilage destruction and osteophyte size. Therapeutic neutralization of CCL17 and Jmjd3 ameliorated both pain and disease, whereas the COX-2 inhibitor only ameliorated pain. In the synovium Ccl17 mRNA was expressed only in the macrophages in a GM-CSF-dependent and IRF4-dependent manner. Conclusions: The GM-CSF?Jmjd3?IRF4?CCL17 pathway is important for the development of CiOA, with CCL17 thus being a potential therapeutic target for the treatment of both OA pain and disease. Electronic supplementary material: The online version of this article (10.1186/s13075-018-1560-9) contains supplementary material, which is available to authorized users. äCCL17 blockade as a therapy for osteoarthritis pain and disease (epmc).pdf DeepDyve Pubget Overpricing