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10.1186/ar4544 http://scihub22266oqcxt.onion/10.1186/ar4544 C4060547!4060547 !24742125     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24742125 &cmd=llinks): Failed to open stream: HTTP request failed! 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Interleukin-10 attenuation of collagen-induced arthritis is associated with suppression of interleukin-17 and retinoid-related orphan receptor ?t production in macrophages and repression of classically activated macrophages |pdf=|usr=}}{{24742125 }} gab.com Text Interleukin-10 attenuation of collagen-induced arthritis is associated with suppression of interleukin-17 and retinoid-related orphan receptor t production in macrophages and repression of classically activated macrophages JO: Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=24742125 #FOAvip INTRODUCTION: Our objective in the present study was to determine the signaling pathway of interleukin 10 (IL-10) for modulating IL-17 expression in macrophages and the importance of this mediation in collagen-induced arthritis (CIA). METHODS: IL-10-knockout (IL-10?/?) mice and wild-type (WT) mice were immunized with chicken type II collagen (CII) to induce arthritis. The expression levels of IL-17 and retinoid-related orphan receptor ?t (ROR?t) in macrophages and joint tissues of IL-10?/? and WT mice were analyzed by enzyme-linked immunosorbent assay, quantitative RT-PCR (qRT-PCR) and Western blotting. The F4/80 macrophages and positive IL-17-producing macrophages in synovial tissues of the mice were determined by immunohistochemistry. The populations of classically activated macrophage (M1) and alternatively activated macrophage (M2) phenotypes were analyzed by flow cytometry. The expression of genes associated with M1 and M2 markers was analyzed by qRT-PCR. RESULTS: Compared to WT mice, IL-10?/? mice had exacerbated CIA development, which was associated with increased production of T helper 17 cell (Th17)/Th1 proinflammatory cytokines and CII-specific immunoglobulin G2a antibody after CII immunization. Macrophages in IL-10?/? mice had increased amounts of IL-17 and ROR?t compared with the amounts in WT mice with CIA. Immunofluorescence microscopy showed that the number of IL-17-producing macrophages in synovial tissues was significantly higher in IL-10?/? mice than in WT mice. IL-10 deficiency might promote macrophage polarization toward the proinflammatory M1 phenotype, which contributes to the rheumatoid arthritis inflammation response. CONCLUSION: IL-10 inhibits IL-17 and ROR?t expression in macrophages and suppresses macrophages toward the proinflammatory M1 phenotype, which is important for the role of IL-10 in mediating the pathogenesis of CIA. Twit Text FOAVip Interleukin-10 attenuation of collagen-induced arthritis is associated with suppression of interleukin-17 and retinoid-related orphan receptor t production in macrophages and repression of classically activated macrophages ????Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=24742125 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24742125 #FOAvip English Wikipedia <ref>{{Cite pmid|24742125 }}</ref> Interleukin-10 attenuation of collagen-induced arthritis is associated with suppression of interleukin-17 and retinoid-related orphan receptor ?t production in macrophages and repression of classically activated macrophages #MMPMID24742125 Ye L ; Wen Z ; Li Y ; Chen B ; Yu T ; Liu L ; Zhang J ; Ma Y ; Xiao S ; Ding L ; Li L ; Huang Z Arthritis Res Ther 2014[Apr]; 16 (2 ): R96 PMID24742125 show ga INTRODUCTION: Our objective in the present study was to determine the signaling pathway of interleukin 10 (IL-10) for modulating IL-17 expression in macrophages and the importance of this mediation in collagen-induced arthritis (CIA). METHODS: IL-10-knockout (IL-10?/?) mice and wild-type (WT) mice were immunized with chicken type II collagen (CII) to induce arthritis. The expression levels of IL-17 and retinoid-related orphan receptor ?t (ROR?t) in macrophages and joint tissues of IL-10?/? and WT mice were analyzed by enzyme-linked immunosorbent assay, quantitative RT-PCR (qRT-PCR) and Western blotting. The F4/80 macrophages and positive IL-17-producing macrophages in synovial tissues of the mice were determined by immunohistochemistry. The populations of classically activated macrophage (M1) and alternatively activated macrophage (M2) phenotypes were analyzed by flow cytometry. The expression of genes associated with M1 and M2 markers was analyzed by qRT-PCR. RESULTS: Compared to WT mice, IL-10?/? mice had exacerbated CIA development, which was associated with increased production of T helper 17 cell (Th17)/Th1 proinflammatory cytokines and CII-specific immunoglobulin G2a antibody after CII immunization. Macrophages in IL-10?/? mice had increased amounts of IL-17 and ROR?t compared with the amounts in WT mice with CIA. Immunofluorescence microscopy showed that the number of IL-17-producing macrophages in synovial tissues was significantly higher in IL-10?/? mice than in WT mice. IL-10 deficiency might promote macrophage polarization toward the proinflammatory M1 phenotype, which contributes to the rheumatoid arthritis inflammation response. CONCLUSION: IL-10 inhibits IL-17 and ROR?t expression in macrophages and suppresses macrophages toward the proinflammatory M1 phenotype, which is important for the role of IL-10 in mediating the pathogenesis of CIA. |Animals [MESH] |Arthritis, Experimental/immunology [MESH] |Arthritis, Rheumatoid/*immunology [MESH] |Blotting, Western [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Flow Cytometry [MESH] |Immunohistochemistry [MESH] |Interleukin-10/*immunology [MESH] |Interleukin-17/*immunology [MESH] |Macrophages/*immunology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Microscopy, Confocal [MESH] |Microscopy, Fluorescence [MESH] |Nuclear Receptor Subfamily 1, Group F, Member 3/*immunology [MESH] |Real-Time Polymerase Chain Reaction [MESH]Interleukin-10 attenuation of collagen-induced arthritis is associated(epmc).pdf DeepDyve Pubget Overpricing