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10.1038/s41598-017-08935-6 http://scihub22266oqcxt.onion/10.1038/s41598-017-08935-6 C5567121!5567121 !28827539     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28827539 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Rep 2017 ; 7 (1 ): 8933 Nephropedia Template TP {{tp|p=28827539 |t=2017. T cell specific Cxcr5 deficiency prevents rheumatoid arthritis |pdf=|usr=}}{{28827539 }} gab.com Text T cell specific Cxcr5 deficiency prevents rheumatoid arthritis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28827539 #FOAvip The chemokine receptor CXCR5 is primarily expressed on B cells and Tfh cells and facilitates their migration towards B cell follicles. In the present study we investigated the role of the CXCL13/CXCR5 axis in the pathogenesis of rheumatoid arthritis (RA) and specifically addressed the impact of CXCR5-mediated T and B cell migration in this disease. Employing collagen-induced arthritis (CIA) we identify CXCR5 as an absolutely essential factor for the induction of inflammatory autoimmune arthritis. Cxcr5-deficient mice and mice selectively lacking Cxcr5 on T cells were completely resistant to CIA, showed impaired germinal center responses and failed to mount an IgG1 antibody response to collagen II. Selective ablation of CXCR5 expression in B cells also led to suppression of CIA owing to diminished GC responses in secondary lymphoid organs (SLO) and impaired anti-collagen II antibody production. Chimeric mice harboring Cxcr5-proficient and Cxcr5-deficient immune cells revealed SLO and not the synovial tissue as the compartment where CXCR5-mediated cell migration induces autoimmune inflammation in arthritis. Thus our data demonstrate that CXCR5-mediated co-localization of Tfh cells and B cells in SLOs is absolutely essential for the induction of RA and identify CXCR5 and Tfh cells as promising therapeutic targets for the treatment of RA. Twit Text FOAVip T cell specific Cxcr5 deficiency prevents rheumatoid arthritis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28827539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28827539 #FOAvip English Wikipedia <ref>{{Cite pmid|28827539 }}</ref> T cell specific Cxcr5 deficiency prevents rheumatoid arthritis #MMPMID28827539 Moschovakis GL ; Bubke A ; Friedrichsen M ; Falk CS ; Feederle R ; Förster R Sci Rep 2017[Aug]; 7 (1 ): 8933 PMID28827539 show ga The chemokine receptor CXCR5 is primarily expressed on B cells and Tfh cells and facilitates their migration towards B cell follicles. In the present study we investigated the role of the CXCL13/CXCR5 axis in the pathogenesis of rheumatoid arthritis (RA) and specifically addressed the impact of CXCR5-mediated T and B cell migration in this disease. Employing collagen-induced arthritis (CIA) we identify CXCR5 as an absolutely essential factor for the induction of inflammatory autoimmune arthritis. Cxcr5-deficient mice and mice selectively lacking Cxcr5 on T cells were completely resistant to CIA, showed impaired germinal center responses and failed to mount an IgG1 antibody response to collagen II. Selective ablation of CXCR5 expression in B cells also led to suppression of CIA owing to diminished GC responses in secondary lymphoid organs (SLO) and impaired anti-collagen II antibody production. Chimeric mice harboring Cxcr5-proficient and Cxcr5-deficient immune cells revealed SLO and not the synovial tissue as the compartment where CXCR5-mediated cell migration induces autoimmune inflammation in arthritis. Thus our data demonstrate that CXCR5-mediated co-localization of Tfh cells and B cells in SLOs is absolutely essential for the induction of RA and identify CXCR5 and Tfh cells as promising therapeutic targets for the treatment of RA. |Animals [MESH] |Arthritis, Rheumatoid/*genetics/*immunology/pathology [MESH] |B-Lymphocytes/immunology/metabolism [MESH] |Disease Models, Animal [MESH] |Disease Susceptibility [MESH] |Humans [MESH] |Leukocytes/immunology/metabolism/pathology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Organ Specificity/genetics [MESH] |Phenotype [MESH] |Receptors, CXCR5/*deficiency [MESH]T cell specific Cxcr5 deficiency prevents rheumatoid arthritis (epmc).pdf DeepDyve Pubget Overpricing