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10.1093/intimm/dxv067 http://scihub22266oqcxt.onion/10.1093/intimm/dxv067 C4889879!4889879 !26567290     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26567290 &cmd=llinks): Failed to open stream: HTTP request failed! 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Leptin deficiency down-regulates IL-23 production in glomerular podocytes resulting in an attenuated immune response in nephrotoxic serum nephritis |pdf=|usr=}}{{26567290 }} gab.com Text Leptin deficiency down-regulates IL-23 production in glomerular podocytes resulting in an attenuated immune response in nephrotoxic serum nephritis JO: Int Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26567290 #FOAvip Leptin, one of the typical adipokines, is reported to promote Th17 cell responses and to enhance production of proinflammatory cytokines. To clarify the role of leptin in the regulation of the IL-23/IL-17 axis and the development of kidney disease, we used a murine model of nephrotoxic serum (NTS) nephritis (NTN). Sheep NTS was administered in wild-type C57BL/6J mice and food-restricted, leptin-deficient C57BL/6J-ob/ob(FR-ob/ob) mice after preimmunization with sheep IgG. The profile of mRNA expression relevant to T helper lymphocytes in the kidneys was analyzed by quantitative real-time PCR (qRT-PCR). Cultured murine glomerular podocytes and peritoneal exudate macrophages (PEMs) were used to investigate the direct effect of leptin on IL-23 or MCP-1 production by qRT-PCR. Kidney injury and macrophage infiltration were significantly attenuated in FR-ob/obmice 7 days after NTS injection. The Th17-dependent secondary immune response against deposited NTS in the glomeruli was totally impaired in FR-ob/obmice because of deteriorated IL-17 and proinflammatory cytokine production including IL-23 and MCP-1 in the kidney. IL-23 was produced in glomerular podocytes in NTN mice and cultured murine glomerular podocytes produced IL-23 under leptin stimulation. MCP-1 production in PEMs was also promoted by leptin. Induction of MCP-1 expression was observed in PEMs regardless of Ob-Rb, and the leptin signal was transduced without STAT3 phosphorylation in PEMs. Leptin deficiency impairs the secondary immune response against NTS and down-regulates IL-23 production and Th17 responses in the NTN kidney, which is accompanied by decreased MCP-1 production and macrophage infiltration in the NTN kidney. Twit Text FOAVip Leptin deficiency down-regulates IL-23 production in glomerular podocytes resulting in an attenuated immune response in nephrotoxic serum nephritis ????Int Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26567290 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26567290 #FOAvip English Wikipedia <ref>{{Cite pmid|26567290 }}</ref> Leptin deficiency down-regulates IL-23 production in glomerular podocytes resulting in an attenuated immune response in nephrotoxic serum nephritis #MMPMID26567290 Goto K ; Kaneko Y ; Sato Y ; Otsuka T ; Yamamoto S ; Goto S ; Yamamoto K ; Yamamoto T ; Kawachi H ; Madaio MP ; Narita I Int Immunol 2016[Apr]; 28 (4 ): 197-208 PMID26567290 show ga Leptin, one of the typical adipokines, is reported to promote Th17 cell responses and to enhance production of proinflammatory cytokines. To clarify the role of leptin in the regulation of the IL-23/IL-17 axis and the development of kidney disease, we used a murine model of nephrotoxic serum (NTS) nephritis (NTN). Sheep NTS was administered in wild-type C57BL/6J mice and food-restricted, leptin-deficient C57BL/6J-ob/ob(FR-ob/ob) mice after preimmunization with sheep IgG. The profile of mRNA expression relevant to T helper lymphocytes in the kidneys was analyzed by quantitative real-time PCR (qRT-PCR). Cultured murine glomerular podocytes and peritoneal exudate macrophages (PEMs) were used to investigate the direct effect of leptin on IL-23 or MCP-1 production by qRT-PCR. Kidney injury and macrophage infiltration were significantly attenuated in FR-ob/obmice 7 days after NTS injection. The Th17-dependent secondary immune response against deposited NTS in the glomeruli was totally impaired in FR-ob/obmice because of deteriorated IL-17 and proinflammatory cytokine production including IL-23 and MCP-1 in the kidney. IL-23 was produced in glomerular podocytes in NTN mice and cultured murine glomerular podocytes produced IL-23 under leptin stimulation. MCP-1 production in PEMs was also promoted by leptin. Induction of MCP-1 expression was observed in PEMs regardless of Ob-Rb, and the leptin signal was transduced without STAT3 phosphorylation in PEMs. Leptin deficiency impairs the secondary immune response against NTS and down-regulates IL-23 production and Th17 responses in the NTN kidney, which is accompanied by decreased MCP-1 production and macrophage infiltration in the NTN kidney. |Animals [MESH] |Biopsy [MESH] |Cell Line [MESH] |Chemokine CCL2/genetics/metabolism [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Gene Expression [MESH] |Immunoglobulin G/blood/immunology [MESH] |Immunophenotyping [MESH] |Interleukin-23/*biosynthesis/genetics [MESH] |Kidney Glomerulus/immunology/metabolism/pathology [MESH] |Leptin/*deficiency [MESH] |Macrophages, Peritoneal/immunology/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Nephritis/*etiology/*metabolism/pathology [MESH] |Podocytes/*metabolism [MESH] |Severity of Illness Index [MESH] |Signal Transduction [MESH]Leptin deficiency down-regulates IL-23 production in glomerular podocy(epmc).pdf DeepDyve Pubget Overpricing