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10.1084/jem.20132307 http://scihub22266oqcxt.onion/10.1084/jem.20132307 C4612100!4612100 !26417004     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26417004 &cmd=llinks): Failed to open stream: HTTP request failed! 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Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis |pdf=|usr=}}{{26417004 }} gab.com Text Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=26417004 #FOAvip Ectopic lymphoid-like structures (ELSs) reminiscent of secondary lymphoid organs often develop at sites of chronic inflammation where they contribute to immune-mediated pathology. Through evaluation of synovial tissues from rheumatoid arthritis (RA) patients, we now show that low interleukin-27 (IL-27) expression corresponds with an increased incidence of ELS and gene signatures associated with their development and activity. The presence of synovial ELS was also noted in mice deficient in the IL-27 receptor (IL-27R) after the onset of inflammatory arthritis. Here, pathology was associated with increased synovial expression of pro-inflammatory cytokines, homeostatic chemokines, and transcriptional regulators linked with lymphoid neogenesis. In both clinical and experimental RA, synovial ELS coincided with the heightened local expression of cytokines and transcription factors of the Th17 and T follicular helper (Tfh) cell lineages, and included podoplanin-expressing T cells within lymphoid aggregates. IL-27 inhibited the differentiation of podoplanin-expressing Th17 cells, and an increased number of these cells were observed in IL-27R-deficient mice with inflammatory arthritis. Thus, IL-27 appears to negatively regulate ELS development in RA through control of effector T cells. These studies open new opportunities for patient stratification and treatment. Twit Text FOAVip Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=26417004 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26417004 #FOAvip English Wikipedia <ref>{{Cite pmid|26417004 }}</ref> Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis #MMPMID26417004 Jones GW ; Bombardieri M ; Greenhill CJ ; McLeod L ; Nerviani A ; Rocher-Ros V ; Cardus A ; Williams AS ; Pitzalis C ; Jenkins BJ ; Jones SA J Exp Med 2015[Oct]; 212 (11 ): 1793-802 PMID26417004 show ga Ectopic lymphoid-like structures (ELSs) reminiscent of secondary lymphoid organs often develop at sites of chronic inflammation where they contribute to immune-mediated pathology. Through evaluation of synovial tissues from rheumatoid arthritis (RA) patients, we now show that low interleukin-27 (IL-27) expression corresponds with an increased incidence of ELS and gene signatures associated with their development and activity. The presence of synovial ELS was also noted in mice deficient in the IL-27 receptor (IL-27R) after the onset of inflammatory arthritis. Here, pathology was associated with increased synovial expression of pro-inflammatory cytokines, homeostatic chemokines, and transcriptional regulators linked with lymphoid neogenesis. In both clinical and experimental RA, synovial ELS coincided with the heightened local expression of cytokines and transcription factors of the Th17 and T follicular helper (Tfh) cell lineages, and included podoplanin-expressing T cells within lymphoid aggregates. IL-27 inhibited the differentiation of podoplanin-expressing Th17 cells, and an increased number of these cells were observed in IL-27R-deficient mice with inflammatory arthritis. Thus, IL-27 appears to negatively regulate ELS development in RA through control of effector T cells. These studies open new opportunities for patient stratification and treatment. |Animals [MESH] |Arthritis, Rheumatoid/*immunology/*pathology [MESH] |Cells, Cultured [MESH] |Humans [MESH] |Interleukins/*physiology [MESH] |Lymphoid Tissue/*pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Receptors, Interleukin/analysis [MESH] |STAT3 Transcription Factor/physiology [MESH]Interleukin-27 inhibits ectopic lymphoid-like structure development in(epmc).pdf DeepDyve Pubget Overpricing