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10.1053/j.gastro.2014.02.010 http://scihub22266oqcxt.onion/10.1053/j.gastro.2014.02.010 C4035425!4035425 !24560868     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24560868 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Gastroenterology 2014 ; 146 (7 ): 1752-62.e4 Nephropedia Template TP {{tp|p=24560868 |t=2014. The tumor necrosis factor family member TNFSF14 (LIGHT) is required for resolution of intestinal inflammation in mice |pdf=|usr=}}{{24560868 }} gab.com Text The tumor necrosis factor family member TNFSF14 (LIGHT) is required for resolution of intestinal inflammation in mice JO: Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=24560868 #FOAvip BACKGROUND & AIMS: The pathogenesis of inflammatory bowel disease (IBD) is associated with a dysregulated mucosal immune response. Expression of the tumor necrosis factor (TNF) superfamily member 14 (TNFSF14, also known as LIGHT [homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes]) on T cells is involved in their activation; transgenic expression of LIGHT on T cells in mice promotes inflammation in multiple organs, including intestine. We investigated the roles for LIGHT in recovery from intestinal inflammation in mice. METHODS: We studied the role of LIGHT in intestinal inflammation using Tnfsf14(-/-) and wild-type mice. Colitis was induced by transfer of CD4(+)CD45RB(high) T cells into Rag1(-/-) or Tnfsf14(-/-)Rag1(-/-) mice, or by administration of dextran sulfate sodium to Tnfsf14(-/-) or wild-type C57BL/6J mice. Mice were weighed, colon tissues were collected and measured, and histology analyses were performed. We measured infiltrating cell populations and expression of cytokines, chemokines, and LIGHT. RESULTS: After administration of dextran sulfate sodium, Tnfsf14(-/-) mice developed more severe colitis than controls, based on their reduced survival, accelerated loss of body weight, and histologic scores. LIGHT protected mice from colitis via the lymphotoxin ? receptor and was expressed mainly by myeloid cells in the colon. Colons of Tnfsf14(-/-) mice also had increased accumulation of innate immune cells and higher levels of cytokines than colons from control mice. LIGHT, therefore, appears to regulate inflammation in the colon. CONCLUSIONS: Tnfsf14(-/-) mice develop more severe colitis than control mice. LIGHT signals through the lymphotoxin ? receptor in the colon to regulate the innate immune response and mediate recovery from intestinal inflammation. Twit Text FOAVip The tumor necrosis factor family member TNFSF14 (LIGHT) is required for resolution of intestinal inflammation in mice ????Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=24560868 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24560868 #FOAvip English Wikipedia <ref>{{Cite pmid|24560868 }}</ref> The tumor necrosis factor family member TNFSF14 (LIGHT) is required for resolution of intestinal inflammation in mice #MMPMID24560868 Krause P ; Zahner SP ; Kim G ; Shaikh RB ; Steinberg MW ; Kronenberg M Gastroenterology 2014[Jun]; 146 (7 ): 1752-62.e4 PMID24560868 show ga BACKGROUND & AIMS: The pathogenesis of inflammatory bowel disease (IBD) is associated with a dysregulated mucosal immune response. Expression of the tumor necrosis factor (TNF) superfamily member 14 (TNFSF14, also known as LIGHT [homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes]) on T cells is involved in their activation; transgenic expression of LIGHT on T cells in mice promotes inflammation in multiple organs, including intestine. We investigated the roles for LIGHT in recovery from intestinal inflammation in mice. METHODS: We studied the role of LIGHT in intestinal inflammation using Tnfsf14(-/-) and wild-type mice. Colitis was induced by transfer of CD4(+)CD45RB(high) T cells into Rag1(-/-) or Tnfsf14(-/-)Rag1(-/-) mice, or by administration of dextran sulfate sodium to Tnfsf14(-/-) or wild-type C57BL/6J mice. Mice were weighed, colon tissues were collected and measured, and histology analyses were performed. We measured infiltrating cell populations and expression of cytokines, chemokines, and LIGHT. RESULTS: After administration of dextran sulfate sodium, Tnfsf14(-/-) mice developed more severe colitis than controls, based on their reduced survival, accelerated loss of body weight, and histologic scores. LIGHT protected mice from colitis via the lymphotoxin ? receptor and was expressed mainly by myeloid cells in the colon. Colons of Tnfsf14(-/-) mice also had increased accumulation of innate immune cells and higher levels of cytokines than colons from control mice. LIGHT, therefore, appears to regulate inflammation in the colon. CONCLUSIONS: Tnfsf14(-/-) mice develop more severe colitis than control mice. LIGHT signals through the lymphotoxin ? receptor in the colon to regulate the innate immune response and mediate recovery from intestinal inflammation. |Animals [MESH] |CD4-Positive T-Lymphocytes/immunology/*metabolism/pathology/transplantation [MESH] |Colitis/chemically induced/immunology/*metabolism/pathology/prevention & control [MESH] |Colon/immunology/*metabolism/pathology [MESH] |Cytokines/metabolism [MESH] |Dextran Sulfate [MESH] |Disease Models, Animal [MESH] |Homeodomain Proteins/genetics/metabolism [MESH] |Immunity, Innate [MESH] |Inflammation Mediators/metabolism [MESH] |Intestinal Mucosa/immunology/*metabolism/pathology [MESH] |Leukocyte Common Antigens/metabolism [MESH] |Lymphotoxin beta Receptor/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Severity of Illness Index [MESH] |Signal Transduction [MESH] |Time Factors [MESH] |Tumor Necrosis Factor Ligand Superfamily Member 14/deficiency/genetics/*metabolism [MESH]The tumor necrosis factor family member TNFSF14 (LIGHT) is required fo(epmc).pdf DeepDyve Pubget Overpricing