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10.1172/JCI82124 http://scihub22266oqcxt.onion/10.1172/JCI82124 C4588300!4588300!26301812     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2015 ; 125 (9): 3692-703 Nephropedia Template TP {{tp|p=26301812|t=2015. Plasmacytoid dendritic cells promote HIV-1?induced group 3 innate lymphoid cell depletion |pdf=|usr=}}{{26301812}} gab.com Text Plasmacytoid dendritic cells promote HIV-1 induced group 3 innate lymphoid cell depletion JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26301812 #FOAvip Group 3 innate lymphoid cells (ILC3s) have demonstrated roles in promoting antibacterial immunity, maintaining epithelial barrier function, and supporting tissue repair. ILC3 alterations are associated with chronic inflammation and inflammatory disease; however, the characteristics and relevant regulatory mechanisms of this cell population in HIV-1 infection are poorly understood due in part to a lack of a robust model. Here, we determined that functional human ILC3s develop in lymphoid organs of humanized mice and that persistent HIV-1 infection in this model depletes ILC3s, as observed in chronic HIV-1?infected patients. In HIV-1?infected mice, effective antiretroviral therapy reversed the loss of ILC3s. HIV-1?dependent reduction of ILC3s required plasmacytoid dendritic cells (pDCs), IFN-I, and the CD95/FasL pathway, as targeted depletion or blockade of these prevented HIV-1?induced ILC3 depletion in vivo and in vitro, respectively. Finally, we determined that HIV-1 infection induces CD95 expression on ILC3s via a pDC- and IFN-I?dependent mechanism that sensitizes ILC3s to undergo CD95/FasL-mediated apoptosis. We conclude that chronic HIV-1 infection depletes ILC3s through pDC activation, induction of IFN-I, and CD95-mediated apoptosis. Twit Text FOAVip Plasmacytoid dendritic cells promote HIV-1 induced group 3 innate lymphoid cell depletion ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26301812 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26301812 #FOAvip English Wikipedia <ref>{{Cite pmid|26301812}}</ref> Plasmacytoid dendritic cells promote HIV-1?induced group 3 innate lymphoid cell depletion #MMPMID26301812 Zhang Z; Cheng L; Zhao J; Li G; Zhang L; Chen W; Nie W; Reszka-Blanco NJ; Wang FS; Su L J Clin Invest 2015[Sep]; 125 (9): 3692-703 PMID26301812show ga Group 3 innate lymphoid cells (ILC3s) have demonstrated roles in promoting antibacterial immunity, maintaining epithelial barrier function, and supporting tissue repair. ILC3 alterations are associated with chronic inflammation and inflammatory disease; however, the characteristics and relevant regulatory mechanisms of this cell population in HIV-1 infection are poorly understood due in part to a lack of a robust model. Here, we determined that functional human ILC3s develop in lymphoid organs of humanized mice and that persistent HIV-1 infection in this model depletes ILC3s, as observed in chronic HIV-1?infected patients. In HIV-1?infected mice, effective antiretroviral therapy reversed the loss of ILC3s. HIV-1?dependent reduction of ILC3s required plasmacytoid dendritic cells (pDCs), IFN-I, and the CD95/FasL pathway, as targeted depletion or blockade of these prevented HIV-1?induced ILC3 depletion in vivo and in vitro, respectively. Finally, we determined that HIV-1 infection induces CD95 expression on ILC3s via a pDC- and IFN-I?dependent mechanism that sensitizes ILC3s to undergo CD95/FasL-mediated apoptosis. We conclude that chronic HIV-1 infection depletes ILC3s through pDC activation, induction of IFN-I, and CD95-mediated apoptosis. äPlasmacytoid dendritic cells promote HIV-1?induced group 3 innate lymp(epmc).pdf DeepDyve Pubget Overpricing