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10.1186/s13578-018-0229-z http://scihub22266oqcxt.onion/10.1186/s13578-018-0229-z C5907314!5907314!29713453     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Biosci 2018 ; 8 (ä): ä Nephropedia Template TP {{tp|p=29713453|t=2018. Anti-CTLA-4 antibodies in cancer immunotherapy: selective depletion of intratumoral regulatory T cells or checkpoint blockade?|pdf=|usr=}}{{29713453}} gab.com Text Anti-CTLA-4 antibodies in cancer immunotherapy: selective depletion of intratumoral regulatory T cells or checkpoint blockade JO: Cell Biosci http://www.kidney.de/pget.php?&tw=1&pmid=29713453 #FOAvip Antibodies to human CTLA-4 have been shown to induce long-lasting protection against melanoma. It is assumed that these antibodies cause tumor rejection by blocking negative signaling from the B7-CTLA-4 interactions to enhance priming of naïve T cells in the lymphoid organs. Recently, we reported that anti-CTLA-4 antibody Ipilimumab effectively induces tumor rejection in vivo although it blocks neither B7 transendocytosis by CTLA-4 nor CTLA-4 binding to immobilized or cell-associated B7. Using genetic model in which the anti-CTLA-4 antibodies are unable to engage more than 50% of CTLA-4, we demonstrated that saturating binding of CTLA-4 is not necessary for tumor rejection. Our results argue against B7-CTLA-4 blockade as the mechanism of action for the clinically effective Ipilimumab. Moreover, Ipilimumab induces tumor rejection even in the absence of de novo T cell priming in the lymphoid organs. Thus, our data are inconsistent with key provisions of the prevailing hypothesis on mechanism of action by anti-CTLA-4 antibodies. Furthermore, anti-CTLA-4 antibodies effectively induce depletion of regulatory T (Treg) cells in tumor microenvironment but not in the peripheral lymphoid organs, which is strictly dependent on Fc receptor on host cells. Based on these data and other recent publications on the subject, we propose that anti-human CTLA-4 antibodies induce tumor rejection by selective depletion of Tregs in the tumors rather than blockade of B7-CTLA-4 interaction in lymphoid organs. Twit Text FOAVip Anti-CTLA-4 antibodies in cancer immunotherapy: selective depletion of intratumoral regulatory T cells or checkpoint blockade ????Cell Biosci http://www.kidney.de/pget.php?&tw=1&pmid=29713453 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29713453 #FOAvip English Wikipedia <ref>{{Cite pmid|29713453}}</ref> Anti-CTLA-4 antibodies in cancer immunotherapy: selective depletion of intratumoral regulatory T cells or checkpoint blockade? #MMPMID29713453 Tang F; Du X; Liu M; Zheng P; Liu Y Cell Biosci 2018[]; 8 (ä): ä PMID29713453show ga Antibodies to human CTLA-4 have been shown to induce long-lasting protection against melanoma. It is assumed that these antibodies cause tumor rejection by blocking negative signaling from the B7-CTLA-4 interactions to enhance priming of naïve T cells in the lymphoid organs. Recently, we reported that anti-CTLA-4 antibody Ipilimumab effectively induces tumor rejection in vivo although it blocks neither B7 transendocytosis by CTLA-4 nor CTLA-4 binding to immobilized or cell-associated B7. Using genetic model in which the anti-CTLA-4 antibodies are unable to engage more than 50% of CTLA-4, we demonstrated that saturating binding of CTLA-4 is not necessary for tumor rejection. Our results argue against B7-CTLA-4 blockade as the mechanism of action for the clinically effective Ipilimumab. Moreover, Ipilimumab induces tumor rejection even in the absence of de novo T cell priming in the lymphoid organs. Thus, our data are inconsistent with key provisions of the prevailing hypothesis on mechanism of action by anti-CTLA-4 antibodies. Furthermore, anti-CTLA-4 antibodies effectively induce depletion of regulatory T (Treg) cells in tumor microenvironment but not in the peripheral lymphoid organs, which is strictly dependent on Fc receptor on host cells. Based on these data and other recent publications on the subject, we propose that anti-human CTLA-4 antibodies induce tumor rejection by selective depletion of Tregs in the tumors rather than blockade of B7-CTLA-4 interaction in lymphoid organs. äAnti-CTLA-4 antibodies in cancer immunotherapy: selective depletion of(epmc).pdf DeepDyve Pubget Overpricing