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10.1128/MCB.00518-15 http://scihub22266oqcxt.onion/10.1128/MCB.00518-15 C4573708!4573708 !26240279     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 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\26240279 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cell+Biol 2015 ; 35 (20 ): 3528-46 Nephropedia Template TP {{tp|p=26240279 |t=2015. Immunosuppression-Independent Role of Regulatory T Cells against Hypertension-Driven Renal Dysfunctions |pdf=|usr=}}{{26240279 }} gab.com Text Immunosuppression-Independent Role of Regulatory T Cells against Hypertension-Driven Renal Dysfunctions JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26240279 #FOAvip Hypertension-associated cardiorenal diseases represent one of the heaviest burdens for current health systems. In addition to hemodynamic damage, recent results have revealed that hematopoietic cells contribute to the development of these diseases by generating proinflammatory and profibrotic environments in the heart and kidney. However, the cell subtypes involved remain poorly characterized. Here we report that CD39(+) regulatory T (TREG) cells utilize an immunosuppression-independent mechanism to counteract renal and possibly cardiac damage during angiotensin II (AngII)-dependent hypertension. This mechanism relies on the direct apoptosis of tissue-resident neutrophils by the ecto-ATP diphosphohydrolase activity of CD39. In agreement with this, experimental and genetic alterations in TREG/TH cell ratios have a direct impact on tissue-resident neutrophil numbers, cardiomyocyte hypertrophy, cardiorenal fibrosis, and, to a lesser extent, arterial pressure elevation during AngII-driven hypertension. These results indicate that TREG cells constitute a first protective barrier against hypertension-driven tissue fibrosis and, in addition, suggest new therapeutic avenues to prevent hypertension-linked cardiorenal diseases. Twit Text FOAVip Immunosuppression-Independent Role of Regulatory T Cells against Hypertension-Driven Renal Dysfunctions ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26240279 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26240279 #FOAvip English Wikipedia <ref>{{Cite pmid|26240279 }}</ref> Immunosuppression-Independent Role of Regulatory T Cells against Hypertension-Driven Renal Dysfunctions #MMPMID26240279 Fabbiano S ; Menacho-Márquez M ; Robles-Valero J ; Pericacho M ; Matesanz-Marín A ; García-Macías C ; Sevilla MA ; Montero MJ ; Alarcón B ; López-Novoa JM ; Martín P ; Bustelo XR Mol Cell Biol 2015[Oct]; 35 (20 ): 3528-46 PMID26240279 show ga Hypertension-associated cardiorenal diseases represent one of the heaviest burdens for current health systems. In addition to hemodynamic damage, recent results have revealed that hematopoietic cells contribute to the development of these diseases by generating proinflammatory and profibrotic environments in the heart and kidney. However, the cell subtypes involved remain poorly characterized. Here we report that CD39(+) regulatory T (TREG) cells utilize an immunosuppression-independent mechanism to counteract renal and possibly cardiac damage during angiotensin II (AngII)-dependent hypertension. This mechanism relies on the direct apoptosis of tissue-resident neutrophils by the ecto-ATP diphosphohydrolase activity of CD39. In agreement with this, experimental and genetic alterations in TREG/TH cell ratios have a direct impact on tissue-resident neutrophil numbers, cardiomyocyte hypertrophy, cardiorenal fibrosis, and, to a lesser extent, arterial pressure elevation during AngII-driven hypertension. These results indicate that TREG cells constitute a first protective barrier against hypertension-driven tissue fibrosis and, in addition, suggest new therapeutic avenues to prevent hypertension-linked cardiorenal diseases. |Angiotensin II/physiology [MESH] |Animals [MESH] |Antigens, CD/metabolism [MESH] |Apoptosis [MESH] |Apyrase/metabolism [MESH] |Cells, Cultured [MESH] |Fibrosis [MESH] |Hypertension/*complications/immunology [MESH] |Immune Tolerance [MESH] |Kidney/immunology/metabolism/pathology [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mice, SCID [MESH] |Neutrophils/physiology [MESH] |Proto-Oncogene Proteins c-vav/genetics/metabolism [MESH] |Renal Insufficiency/etiology/*immunology [MESH] |T-Lymphocytes, Helper-Inducer/physiology [MESH]Immunosuppression-Independent Role of Regulatory T Cells against Hyp(epmc).pdf DeepDyve Pubget Overpricing