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10.1111/cei.12937 http://scihub22266oqcxt.onion/10.1111/cei.12937 C5383436!5383436 !28152566     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28152566 &cmd=llinks): Failed to open stream: HTTP request failed! 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Exacerbation of spontaneous autoimmune nephritis following regulatory T cell depletion in B cell lymphoma 2-interacting mediator knock-out mice |pdf=|usr=}}{{28152566 }} gab.com Text Exacerbation of spontaneous autoimmune nephritis following regulatory T cell depletion in B cell lymphoma 2-interacting mediator knock-out mice JO: Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28152566 #FOAvip Regulatory T cells (T(regs) ) have been recognized as central mediators for maintaining peripheral tolerance and limiting autoimmune diseases. The loss of T(regs) or their function has been associated with exacerbation of autoimmune disease. However, the temporary loss of T(regs) in the chronic spontaneous disease model has not been investigated. In this study, we evaluated the role of T(regs) in a novel chronic spontaneous glomerulonephritis model of B cell lymphoma 2-interacting mediator (Bim) knock-out mice by transient depleting T(regs) . Bim is a pro-apoptotic member of the B cell lymphoma 2 (Bcl-2) family. Bim knock-out (Bim(-/-) ) mice fail to delete autoreactive T cells in thymus, leading to chronic spontaneous autoimmune kidney disease. We found that T(reg) depletion in Bim(-/-) mice exacerbated the kidney injury with increased proteinuria, impaired kidney function, weight loss and greater histological injury compared with wild-type mice. There was a significant increase in interstitial infiltrate of inflammatory cells, antibody deposition and tubular damage. Furthermore, the serum levels of cytokines interleukin (IL)-2, IL-4, IL-6, IL-10, IL-17?, interferon (IFN)-? and tumour necrosis factor (TNF)-? were increased significantly after T(reg) depletion in Bim(-/-) mice. This study demonstrates that transient depletion of T(regs) leads to enhanced self-reactive T effector cell function followed by exacerbation of kidney disease in the chronic spontaneous kidney disease model of Bim-deficient mice. Twit Text FOAVip Exacerbation of spontaneous autoimmune nephritis following regulatory T cell depletion in B cell lymphoma 2-interacting mediator knock-out mice ????Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28152566 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28152566 #FOAvip English Wikipedia <ref>{{Cite pmid|28152566 }}</ref> Exacerbation of spontaneous autoimmune nephritis following regulatory T cell depletion in B cell lymphoma 2-interacting mediator knock-out mice #MMPMID28152566 Wang YM ; Zhang GY ; Wang Y ; Hu M ; Zhou JJ ; Sawyer A ; Cao Q ; Wang Y ; Zheng G ; Lee VW ; Harris DC ; Alexander SI Clin Exp Immunol 2017[May]; 188 (2 ): 195-207 PMID28152566 show ga Regulatory T cells (T(regs) ) have been recognized as central mediators for maintaining peripheral tolerance and limiting autoimmune diseases. The loss of T(regs) or their function has been associated with exacerbation of autoimmune disease. However, the temporary loss of T(regs) in the chronic spontaneous disease model has not been investigated. In this study, we evaluated the role of T(regs) in a novel chronic spontaneous glomerulonephritis model of B cell lymphoma 2-interacting mediator (Bim) knock-out mice by transient depleting T(regs) . Bim is a pro-apoptotic member of the B cell lymphoma 2 (Bcl-2) family. Bim knock-out (Bim(-/-) ) mice fail to delete autoreactive T cells in thymus, leading to chronic spontaneous autoimmune kidney disease. We found that T(reg) depletion in Bim(-/-) mice exacerbated the kidney injury with increased proteinuria, impaired kidney function, weight loss and greater histological injury compared with wild-type mice. There was a significant increase in interstitial infiltrate of inflammatory cells, antibody deposition and tubular damage. Furthermore, the serum levels of cytokines interleukin (IL)-2, IL-4, IL-6, IL-10, IL-17?, interferon (IFN)-? and tumour necrosis factor (TNF)-? were increased significantly after T(reg) depletion in Bim(-/-) mice. This study demonstrates that transient depletion of T(regs) leads to enhanced self-reactive T effector cell function followed by exacerbation of kidney disease in the chronic spontaneous kidney disease model of Bim-deficient mice. |*Lymphocyte Depletion [MESH] |Animals [MESH] |Autoimmune Diseases/*immunology/pathology [MESH] |Bcl-2-Like Protein 11/deficiency/*genetics [MESH] |Cytokines/blood [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Glomerulonephritis/*immunology/pathology/physiopathology [MESH] |Interleukin-10/blood [MESH] |Interleukin-6/blood [MESH] |Kidney/immunology/pathology/physiopathology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Proteinuria [MESH]Exacerbation of spontaneous autoimmune nephritis following regulatory (epmc).pdf DeepDyve Pubget Overpricing