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10.4049/jimmunol.1502581 http://scihub22266oqcxt.onion/10.4049/jimmunol.1502581 C4992601!4992601!27474077     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2016 ; 197 (5): 1733-42 Nephropedia Template TP {{tp|p=27474077|t=2016. NADPH Oxidase-Derived Superoxide Provides a Third Signal for CD4 T cell Effector Responses |pdf=|usr=}}{{27474077}} gab.com Text NADPH Oxidase-Derived Superoxide Provides a Third Signal for CD4 T cell Effector Responses JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27474077 #FOAvip Originally recognized for their direct induced toxicity as a component of the innate immune response, reactive oxygen species (ROS) can profoundly modulate T cell adaptive immune responses. Efficient T cell activation requires: signal 1, consisting of an antigenic peptide-MHC complex binding with the T cell receptor (TCR); signal 2, the interaction of co-stimulatory molecules on T cells and antigen-presenting cells (APC); and signal 3, the generation of innate immune-derived ROS and pro-inflammatory cytokines. This third signal, in particular, has proven essential in generating productive and long-lasting immune responses. Our laboratory previously demonstrated profound antigen-specific hyporesponsiveness in the absence of NADPH-oxidase-derived (NOX) superoxide. To further examine the consequences of ROS deficiency on antigen-specific T cell responses, our laboratory generated the OT-II.Ncf1m1J mouse, possessing superoxide-deficient T cells recognizing the nominal antigen OVA323-339. In this study, we demonstrate that OT-II.Ncf1m1J CD4 T cells displayed a severe reduction in Th1 T cell responses, in addition to blunted IL-12R expression and severely attenuated pro-inflammatory chemokine ligands. Conversely, IFN-? synthesis and IL-12R synthesis were rescued by the addition of exogenous superoxide via the paramagnetic superoxide donor potassium dioxide (KO2) or superoxide-sufficient DCs. Ultimately, this data highlights the importance of NOX-derived ROS in providing a third signal for adaptive immune maturation by modulating IL-12/IL-12R pathway and the novelty of the OT-II.Ncf1m1J mouse model to determine the role of redox-dependent signaling on effector responses. Thus, targeting ROS represents a promising therapeutic strategy in dampening antigen-specific T cell responses and T cell-mediated autoimmune diseases, such as Type 1 diabetes. Twit Text FOAVip NADPH Oxidase-Derived Superoxide Provides a Third Signal for CD4 T cell Effector Responses ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27474077 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27474077 #FOAvip English Wikipedia <ref>{{Cite pmid|27474077}}</ref> NADPH Oxidase-Derived Superoxide Provides a Third Signal for CD4 T cell Effector Responses #MMPMID27474077 Padgett LE; Tse HM J Immunol 2016[Sep]; 197 (5): 1733-42 PMID27474077show ga Originally recognized for their direct induced toxicity as a component of the innate immune response, reactive oxygen species (ROS) can profoundly modulate T cell adaptive immune responses. Efficient T cell activation requires: signal 1, consisting of an antigenic peptide-MHC complex binding with the T cell receptor (TCR); signal 2, the interaction of co-stimulatory molecules on T cells and antigen-presenting cells (APC); and signal 3, the generation of innate immune-derived ROS and pro-inflammatory cytokines. This third signal, in particular, has proven essential in generating productive and long-lasting immune responses. Our laboratory previously demonstrated profound antigen-specific hyporesponsiveness in the absence of NADPH-oxidase-derived (NOX) superoxide. To further examine the consequences of ROS deficiency on antigen-specific T cell responses, our laboratory generated the OT-II.Ncf1m1J mouse, possessing superoxide-deficient T cells recognizing the nominal antigen OVA323-339. In this study, we demonstrate that OT-II.Ncf1m1J CD4 T cells displayed a severe reduction in Th1 T cell responses, in addition to blunted IL-12R expression and severely attenuated pro-inflammatory chemokine ligands. Conversely, IFN-? synthesis and IL-12R synthesis were rescued by the addition of exogenous superoxide via the paramagnetic superoxide donor potassium dioxide (KO2) or superoxide-sufficient DCs. Ultimately, this data highlights the importance of NOX-derived ROS in providing a third signal for adaptive immune maturation by modulating IL-12/IL-12R pathway and the novelty of the OT-II.Ncf1m1J mouse model to determine the role of redox-dependent signaling on effector responses. Thus, targeting ROS represents a promising therapeutic strategy in dampening antigen-specific T cell responses and T cell-mediated autoimmune diseases, such as Type 1 diabetes. äNADPH Oxidase-Derived Superoxide Provides a Third Signal for CD4 T cel(epmc).pdf DeepDyve Pubget Overpricing