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10.1002/eji.201343866 http://scihub22266oqcxt.onion/10.1002/eji.201343866 C4482763!4482763!24448964     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       Eur+J+Immunol 2014 ; 44 (4): 1119-29 Nephropedia Template TP {{tp|p=24448964|t=2014. Physiological control of NKT cell-dependent hepatitis induction by extracellular adenosine |pdf=|usr=}}{{24448964}} gab.com Text Physiological control of NKT cell-dependent hepatitis induction by extracellular adenosine JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24448964 #FOAvip Extracellular adenosine regulates inflammatory responses via A2A adenosine receptor (A2AR). A2AR-deficiency results in much exaggerated acute hepatitis, indicating non-redundancy of adenosine-A2AR pathway in inhibitory mechanisms of immune activation. To identify a critical target of immunoregulatory effect of extracellular adenosine, we focused on NKT cells, which play an indispensable role in hepatitis. A2AR agonist abolished NKT cell-dependent induction of acute hepatitis by Con A or ?-galactosylceramide (?-GalCer), corresponding to down-regulation of activation markers and cytokines in NKT cells and of NK cell co-activation. These results show that A2AR signaling can down-regulate NKT cell activation and suppress NKT cell-triggered inflammatory responses. Next, we hypothesized that NKT cells might be under physiological control of the adenosine-A2AR pathway. Indeed, both Con A and ?-GalCer induced more severe hepatitis in A2AR?/? mice than in wild-type controls. Transfer of A2AR?/? NKT cells into A2AR-expressing recipients resulted in exaggeration of Con A-induced liver damage, suggesting that NKT cell activation is controlled by endogenous adenosine via A2AR, and this physiological regulatory mechanism of NKT cells is critical in the control of tissue-damaging inflammation. The current study suggests the possibility to manipulate NKT cell activity in inflammatory disorders through intervention to the adenosine-A2AR pathway. Twit Text FOAVip Physiological control of NKT cell-dependent hepatitis induction by extracellular adenosine ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24448964 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24448964 #FOAvip English Wikipedia <ref>{{Cite pmid|24448964}}</ref> Physiological control of NKT cell-dependent hepatitis induction by extracellular adenosine #MMPMID24448964 Subramanian M; Kini R; Madasu M; Ohta A; Nowak M; Exley M; Sitkovsky M; Ohta A Eur J Immunol 2014[Apr]; 44 (4): 1119-29 PMID24448964show ga Extracellular adenosine regulates inflammatory responses via A2A adenosine receptor (A2AR). A2AR-deficiency results in much exaggerated acute hepatitis, indicating non-redundancy of adenosine-A2AR pathway in inhibitory mechanisms of immune activation. To identify a critical target of immunoregulatory effect of extracellular adenosine, we focused on NKT cells, which play an indispensable role in hepatitis. A2AR agonist abolished NKT cell-dependent induction of acute hepatitis by Con A or ?-galactosylceramide (?-GalCer), corresponding to down-regulation of activation markers and cytokines in NKT cells and of NK cell co-activation. These results show that A2AR signaling can down-regulate NKT cell activation and suppress NKT cell-triggered inflammatory responses. Next, we hypothesized that NKT cells might be under physiological control of the adenosine-A2AR pathway. Indeed, both Con A and ?-GalCer induced more severe hepatitis in A2AR?/? mice than in wild-type controls. Transfer of A2AR?/? NKT cells into A2AR-expressing recipients resulted in exaggeration of Con A-induced liver damage, suggesting that NKT cell activation is controlled by endogenous adenosine via A2AR, and this physiological regulatory mechanism of NKT cells is critical in the control of tissue-damaging inflammation. The current study suggests the possibility to manipulate NKT cell activity in inflammatory disorders through intervention to the adenosine-A2AR pathway. äPhysiological control of NKT cell-dependent hepatitis induction by ext(epmc).pdf DeepDyve Pubget Overpricing