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10.1371/journal.pone.0178352 http://scihub22266oqcxt.onion/10.1371/journal.pone.0178352 C5446182!5446182 !28552941     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28552941 &cmd=llinks): Failed to open stream: HTTP request failed! 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CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy |pdf=|usr=}}{{28552941 }} gab.com Text CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28552941 #FOAvip IgA nephropathy (IgAN) is the most common primary glomerulonephritis characterized by human mesangial cells (HMC) proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient IgA1. However, how IgA1 contributes to IgAN has yet to be completely elucidated. In this study, the expression profile of chemokines was more altered in IgA1-treated HMC than in the control group. CCL20 was significantly higher either in the serum of IgAN patients or in IgA1-treated HMC. Further experiments demonstrated that CCR6, the only receptor of CCL20, was highly expressed in activated T cells. Intracellular staining assay and cytokine expression profile implied that CCR6+ T cells produced high IL-17 levels. Transwell experiment immunohistochemistry and immunofluorescence experiments extensively demonstrated that CCL20 could recruit inflammatory Th17 cells to the kidneys. These phenomena caused a series of immune inflammatory responses and further damaged the kidneys. Therefore, HMC stimulated by IgA1 could produce CCL20 and consequently recruit inflammatory Th17 cells to the kidneys to induce further lesion in IgA nephropathy. Twit Text FOAVip CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28552941 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28552941 #FOAvip English Wikipedia <ref>{{Cite pmid|28552941 }}</ref> CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy #MMPMID28552941 Lu G ; Zhang X ; Shen L ; Qiao Q ; Li Y ; Sun J ; Zhang J PLoS One 2017[]; 12 (5 ): e0178352 PMID28552941 show ga IgA nephropathy (IgAN) is the most common primary glomerulonephritis characterized by human mesangial cells (HMC) proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient IgA1. However, how IgA1 contributes to IgAN has yet to be completely elucidated. In this study, the expression profile of chemokines was more altered in IgA1-treated HMC than in the control group. CCL20 was significantly higher either in the serum of IgAN patients or in IgA1-treated HMC. Further experiments demonstrated that CCR6, the only receptor of CCL20, was highly expressed in activated T cells. Intracellular staining assay and cytokine expression profile implied that CCR6+ T cells produced high IL-17 levels. Transwell experiment immunohistochemistry and immunofluorescence experiments extensively demonstrated that CCL20 could recruit inflammatory Th17 cells to the kidneys. These phenomena caused a series of immune inflammatory responses and further damaged the kidneys. Therefore, HMC stimulated by IgA1 could produce CCL20 and consequently recruit inflammatory Th17 cells to the kidneys to induce further lesion in IgA nephropathy. |Adult [MESH] |Cells, Cultured [MESH] |Chemokine CCL20/*metabolism [MESH] |Coculture Techniques [MESH] |Female [MESH] |Glomerular Mesangium/*metabolism/pathology [MESH] |Glomerulonephritis, IGA/*immunology [MESH] |Humans [MESH] |Immunoglobulin A/*immunology [MESH] |Lymphocyte Activation [MESH] |Male [MESH] |Middle Aged [MESH] |Real-Time Polymerase Chain Reaction [MESH] |T-Lymphocytes/immunology [MESH] |Th17 Cells/*immunology [MESH]CCL20 secreted from IgA1-stimulated human mesangial cells recruits inf(epmc).pdf DeepDyve Pubget Overpricing