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10.1016/j.immuni.2016.04.015 http://scihub22266oqcxt.onion/10.1016/j.immuni.2016.04.015 C4908967!4908967!27192578     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       Immunity 2016 ; 44 (5): 1190-203 Nephropedia Template TP {{tp|p=27192578|t=2016. PSGL-1 is an immune checkpoint regulator that promotes T cell exhaustion |pdf=|usr=}}{{27192578}} gab.com Text PSGL-1 is an immune checkpoint regulator that promotes T cell exhaustion JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=27192578 #FOAvip Chronic viruses and cancers thwart immune responses in humans by inducing T cell dysfunction. Using a murine chronic virus that models human infections, we investigated the function of the adhesion molecule, P-selectin glycoprotein ligand-1 (PSGL-1) that is upregulated on responding T cells. PSGL-1-deficient mice cleared the virus due to increased intrinsic survival of multifunctional effector T cells that had downregulated PD-1 as well as other inhibitory receptors. Notably, this response resulted in CD4+ T cell-dependent immunopathology. Mechanistically, PSGL-1 ligation on exhausted CD8+ T cells inhibited T cell receptor (TCR) and interleukin-2 (IL-2) signaling, and upregulated PD-1, leading to diminished survival with TCR stimulation. In models of melanoma cancer where T cell dysfunction occurs, PSGL-1-deficiency led to PD-1 downregulation, improved T cell responses, and tumor control. Thus, PSGL-1 plays a fundamental role in balancing viral control and immunopathology, and also functions to regulate T cell responses in the tumor microenvironment. Twit Text FOAVip PSGL-1 is an immune checkpoint regulator that promotes T cell exhaustion ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=27192578 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27192578 #FOAvip English Wikipedia <ref>{{Cite pmid|27192578}}</ref> PSGL-1 is an immune checkpoint regulator that promotes T cell exhaustion #MMPMID27192578 Tinoco R; Carrette F; Barraza ML; Otero DC; Magaņa J; Bosenberg MW; Swain SL; Bradley LM Immunity 2016[May]; 44 (5): 1190-203 PMID27192578show ga Chronic viruses and cancers thwart immune responses in humans by inducing T cell dysfunction. Using a murine chronic virus that models human infections, we investigated the function of the adhesion molecule, P-selectin glycoprotein ligand-1 (PSGL-1) that is upregulated on responding T cells. PSGL-1-deficient mice cleared the virus due to increased intrinsic survival of multifunctional effector T cells that had downregulated PD-1 as well as other inhibitory receptors. Notably, this response resulted in CD4+ T cell-dependent immunopathology. Mechanistically, PSGL-1 ligation on exhausted CD8+ T cells inhibited T cell receptor (TCR) and interleukin-2 (IL-2) signaling, and upregulated PD-1, leading to diminished survival with TCR stimulation. In models of melanoma cancer where T cell dysfunction occurs, PSGL-1-deficiency led to PD-1 downregulation, improved T cell responses, and tumor control. Thus, PSGL-1 plays a fundamental role in balancing viral control and immunopathology, and also functions to regulate T cell responses in the tumor microenvironment. äPSGL-1 is an immune checkpoint regulator that promotes T cell exhausti(epmc).pdf DeepDyve Pubget Overpricing