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10.7554/eLife.30938 http://scihub22266oqcxt.onion/10.7554/eLife.30938 C6025959!6025959!29911570     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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       eLife 2018 ; 7 (ä): ä Nephropedia Template TP {{tp|p=29911570|t=2018. Long-term antigen exposure irreversibly modifies metabolic requirements for T cell function |pdf=|usr=}}{{29911570}} gab.com Text Long-term antigen exposure irreversibly modifies metabolic requirements for T cell function JO: eLife http://www.kidney.de/pget.php?&tw=1&pmid=29911570 #FOAvip Energy metabolism is essential for T cell function. However, how persistent antigenic stimulation affects T cell metabolism is unknown. Here, we report that long-term in vivo antigenic exposure induced a specific deficit in numerous metabolic enzymes. Accordingly, T cells exhibited low basal glycolytic flux and limited respiratory capacity. Strikingly, blockade of inhibitory receptor PD-1 stimulated the production of IFN? in chronic T cells, but failed to shift their metabolism towards aerobic glycolysis, as observed in effector T cells. Instead, chronic T cells appeared to rely on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) to produce ATP for IFN? synthesis. Check-point blockade, however, increased mitochondrial production of superoxide and reduced viability and effector function. Thus, in the absence of a glycolytic switch, PD-1-mediated inhibition appears essential for limiting oxidative metabolism linked to effector function in chronic T cells, thereby promoting survival and functional fitness. Twit Text FOAVip Long-term antigen exposure irreversibly modifies metabolic requirements for T cell function ????eLife http://www.kidney.de/pget.php?&tw=1&pmid=29911570 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29911570 #FOAvip English Wikipedia <ref>{{Cite pmid|29911570}}</ref> Long-term antigen exposure irreversibly modifies metabolic requirements for T cell function #MMPMID29911570 Bettonville M; d'Aria S; Weatherly K; Porporato PE; Zhang J; Bousbata S; Sonveaux P; Braun MY eLife 2018[]; 7 (ä): ä PMID29911570show ga Energy metabolism is essential for T cell function. However, how persistent antigenic stimulation affects T cell metabolism is unknown. Here, we report that long-term in vivo antigenic exposure induced a specific deficit in numerous metabolic enzymes. Accordingly, T cells exhibited low basal glycolytic flux and limited respiratory capacity. Strikingly, blockade of inhibitory receptor PD-1 stimulated the production of IFN? in chronic T cells, but failed to shift their metabolism towards aerobic glycolysis, as observed in effector T cells. Instead, chronic T cells appeared to rely on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) to produce ATP for IFN? synthesis. Check-point blockade, however, increased mitochondrial production of superoxide and reduced viability and effector function. Thus, in the absence of a glycolytic switch, PD-1-mediated inhibition appears essential for limiting oxidative metabolism linked to effector function in chronic T cells, thereby promoting survival and functional fitness. äLong-term antigen exposure irreversibly modifies metabolic requirement(epmc).pdf DeepDyve Pubget Overpricing