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10.15252/emmm.201607176 http://scihub22266oqcxt.onion/10.15252/emmm.201607176 C5452038!5452038!28455312     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2017 ; 9 (6): 835-51 Nephropedia Template TP {{tp|p=28455312|t=2017. Administration of RANKL boosts thymic regeneration upon bone marrow transplantation |pdf=|usr=}}{{28455312}} gab.com Text Administration of RANKL boosts thymic regeneration upon bone marrow transplantation JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28455312 #FOAvip Cytoablative treatments lead to severe damages on thymic epithelial cells (TECs), which result in delayed de novo thymopoiesis and a prolonged period of T?cell immunodeficiency. Understanding the mechanisms that govern thymic regeneration is of paramount interest for the recovery of a functional immune system notably after bone marrow transplantation (BMT). Here, we show that RANK ligand (RANKL) is upregulated in CD4+ thymocytes and lymphoid tissue inducer (LTi) cells during the early phase of thymic regeneration. Importantly, whereas RANKL neutralization alters TEC recovery after irradiation, ex vivo RANKL administration during BMT boosts the regeneration of TEC subsets including thymic epithelial progenitor?enriched cells, thymus homing of lymphoid progenitors, and de novo thymopoiesis. RANKL increases specifically in LTi cells, lymphotoxin ?, which is critical for thymic regeneration. RANKL treatment, dependent on lymphotoxin ?, is beneficial upon BMT in young and aged individuals. This study thus indicates that RANKL may be clinically useful to improve T?cell function recovery after BMT by controlling multiple facets of thymic regeneration. Twit Text FOAVip Administration of RANKL boosts thymic regeneration upon bone marrow transplantation ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28455312 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28455312 #FOAvip English Wikipedia <ref>{{Cite pmid|28455312}}</ref> Administration of RANKL boosts thymic regeneration upon bone marrow transplantation #MMPMID28455312 Lopes N; Vachon H; Marie J; Irla M EMBO Mol Med 2017[Jun]; 9 (6): 835-51 PMID28455312show ga Cytoablative treatments lead to severe damages on thymic epithelial cells (TECs), which result in delayed de novo thymopoiesis and a prolonged period of T?cell immunodeficiency. Understanding the mechanisms that govern thymic regeneration is of paramount interest for the recovery of a functional immune system notably after bone marrow transplantation (BMT). Here, we show that RANK ligand (RANKL) is upregulated in CD4+ thymocytes and lymphoid tissue inducer (LTi) cells during the early phase of thymic regeneration. Importantly, whereas RANKL neutralization alters TEC recovery after irradiation, ex vivo RANKL administration during BMT boosts the regeneration of TEC subsets including thymic epithelial progenitor?enriched cells, thymus homing of lymphoid progenitors, and de novo thymopoiesis. RANKL increases specifically in LTi cells, lymphotoxin ?, which is critical for thymic regeneration. RANKL treatment, dependent on lymphotoxin ?, is beneficial upon BMT in young and aged individuals. This study thus indicates that RANKL may be clinically useful to improve T?cell function recovery after BMT by controlling multiple facets of thymic regeneration. äAdministration of RANKL boosts thymic regeneration upon bone marrow tr(epmc).pdf DeepDyve Pubget Overpricing