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10.1681/ASN.2014090927 http://scihub22266oqcxt.onion/10.1681/ASN.2014090927 C4769185!4769185!26116356     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2016 ; 27 (3): 706-14 Nephropedia Template TP {{tp|p=26116356|t=2016. Endogenous Toll-Like Receptor 9 Regulates AKI by Promoting Regulatory T Cell Recruitment |pdf=|usr=}}{{26116356}} gab.com Text Endogenous Toll-Like Receptor 9 Regulates AKI by Promoting Regulatory T Cell Recruitment JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26116356 #FOAvip Toll-like receptor 9 (TLR9) enhances proinflammatory responses, but whether it can act in a regulatory capacity remains to be established. In experimental murine AKI induced by cisplatin, Tlr9?/? mice developed enhanced renal injury and exhibited fewer intrarenal regulatory T cells (Tregs) compared with genetically intact mice. A series of reconstitution and depletion studies defined a role for TLR9 in maintaining Treg-mediated homeostasis in cisplatin-induced AKI. When Rag1?/? mice were reconstituted with nonregulatory CD25? splenocytes from wild-type (WT) or Tlr9?/? mice, AKI was similarly enhanced. However, when Rag1?/? mice were reconstituted with CD4+CD25+ regulatory cells, WT CD4+CD25+ cells were more renoprotective and localized to the kidney more efficiently than Tlr9?/? CD4+CD25+ cells. In Treg-depleted Foxp3DTR mice, reconstitution with naive WT CD4+CD25+ cells resulted in less severe AKI than did reconstitution with Tlr9?/? Tregs. Tlr9?/? mice were not deficient in CD4+CD25+ cells, and WT and TLR9-deficient Tregs had similar suppressive function ex vivo. However, expression of adhesion molecules important in Treg trafficking was reduced on peripheral CD4+CD25+ cells from Tlr9?/? mice. In conclusion, we identified a pathway by which TLR9 promotes renal Treg accumulation in AKI. Twit Text FOAVip Endogenous Toll-Like Receptor 9 Regulates AKI by Promoting Regulatory T Cell Recruitment ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26116356 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26116356 #FOAvip English Wikipedia <ref>{{Cite pmid|26116356}}</ref> Endogenous Toll-Like Receptor 9 Regulates AKI by Promoting Regulatory T Cell Recruitment #MMPMID26116356 Alikhan MA; Summers SA; Gan PY; Chan AJ; Khouri MB; Ooi JD; Ghali JR; Odobasic D; Hickey MJ; Kitching AR; Holdsworth SR J Am Soc Nephrol 2016[Mar]; 27 (3): 706-14 PMID26116356show ga Toll-like receptor 9 (TLR9) enhances proinflammatory responses, but whether it can act in a regulatory capacity remains to be established. In experimental murine AKI induced by cisplatin, Tlr9?/? mice developed enhanced renal injury and exhibited fewer intrarenal regulatory T cells (Tregs) compared with genetically intact mice. A series of reconstitution and depletion studies defined a role for TLR9 in maintaining Treg-mediated homeostasis in cisplatin-induced AKI. When Rag1?/? mice were reconstituted with nonregulatory CD25? splenocytes from wild-type (WT) or Tlr9?/? mice, AKI was similarly enhanced. However, when Rag1?/? mice were reconstituted with CD4+CD25+ regulatory cells, WT CD4+CD25+ cells were more renoprotective and localized to the kidney more efficiently than Tlr9?/? CD4+CD25+ cells. In Treg-depleted Foxp3DTR mice, reconstitution with naive WT CD4+CD25+ cells resulted in less severe AKI than did reconstitution with Tlr9?/? Tregs. Tlr9?/? mice were not deficient in CD4+CD25+ cells, and WT and TLR9-deficient Tregs had similar suppressive function ex vivo. However, expression of adhesion molecules important in Treg trafficking was reduced on peripheral CD4+CD25+ cells from Tlr9?/? mice. In conclusion, we identified a pathway by which TLR9 promotes renal Treg accumulation in AKI. äEndogenous Toll-Like Receptor 9 Regulates AKI by Promoting Regulatory (epmc).pdf DeepDyve Pubget Overpricing