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10.1126/sciadv.1500415 http://scihub22266oqcxt.onion/10.1126/sciadv.1500415 C4646799!4646799 !26601285     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26601285 &cmd=llinks): Failed to open stream: HTTP request failed! 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Co-potentiation of antigen recognition: A mechanism to boost weak T cell responses and provide immunotherapy in vivo |pdf=|usr=}}{{26601285 }} gab.com Text Co-potentiation of antigen recognition: A mechanism to boost weak T cell responses and provide immunotherapy in vivo JO: Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=26601285 #FOAvip Adaptive immunity is mediated by antigen receptors that can induce weak or strong immune responses depending on the nature of the antigen that is bound. In T lymphocytes, antigen recognition triggers signal transduction by clustering T cell receptor (TCR)/CD3 multiprotein complexes. In addition, it hypothesized that biophysical changes induced in TCR/CD3 that accompany receptor engagement may contribute to signal intensity. Nonclustering monovalent TCR/CD3 engagement is functionally inert despite the fact that it may induce changes in conformational arrangement or in the flexibility of receptor subunits. We report that the intrinsically inert monovalent engagement of TCR/CD3 can specifically enhance physiologic T cell responses to weak antigens in vitro and in vivo without stimulating antigen-unengaged T cells and without interrupting T cell responses to strong antigens, an effect that we term as "co-potentiation." We identified Mono-7D6-Fab, which biophysically altered TCR/CD3 when bound and functionally enhanced immune reactivity to several weak antigens in vitro, including a gp100-derived peptide associated with melanoma. In vivo, Mono-7D6-Fab induced T cell antigen-dependent therapeutic responses against melanoma lung metastases, an effect that synergized with other anti-melanoma immunotherapies to significantly improve outcome and survival. We conclude that Mono-7D6-Fab directly co-potentiated TCR/CD3 engagement by weak antigens and that such concept can be translated into an immunotherapeutic design. The co-potentiation principle may be applicable to other receptors that could be regulated by otherwise inert compounds whose latent potency is only invoked in concert with specific physiologic ligands. Twit Text FOAVip Co-potentiation of antigen recognition: A mechanism to boost weak T cell responses and provide immunotherapy in vivo ????Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=26601285 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26601285 #FOAvip English Wikipedia <ref>{{Cite pmid|26601285 }}</ref> Co-potentiation of antigen recognition: A mechanism to boost weak T cell responses and provide immunotherapy in vivo #MMPMID26601285 Hoffmann MM ; Molina-Mendiola C ; Nelson AD ; Parks CA ; Reyes EE ; Hansen MJ ; Rajagopalan G ; Pease LR ; Schrum AG ; Gil D Sci Adv 2015[Oct]; 1 (9 ): e1500415 PMID26601285 show ga Adaptive immunity is mediated by antigen receptors that can induce weak or strong immune responses depending on the nature of the antigen that is bound. In T lymphocytes, antigen recognition triggers signal transduction by clustering T cell receptor (TCR)/CD3 multiprotein complexes. In addition, it hypothesized that biophysical changes induced in TCR/CD3 that accompany receptor engagement may contribute to signal intensity. Nonclustering monovalent TCR/CD3 engagement is functionally inert despite the fact that it may induce changes in conformational arrangement or in the flexibility of receptor subunits. We report that the intrinsically inert monovalent engagement of TCR/CD3 can specifically enhance physiologic T cell responses to weak antigens in vitro and in vivo without stimulating antigen-unengaged T cells and without interrupting T cell responses to strong antigens, an effect that we term as "co-potentiation." We identified Mono-7D6-Fab, which biophysically altered TCR/CD3 when bound and functionally enhanced immune reactivity to several weak antigens in vitro, including a gp100-derived peptide associated with melanoma. In vivo, Mono-7D6-Fab induced T cell antigen-dependent therapeutic responses against melanoma lung metastases, an effect that synergized with other anti-melanoma immunotherapies to significantly improve outcome and survival. We conclude that Mono-7D6-Fab directly co-potentiated TCR/CD3 engagement by weak antigens and that such concept can be translated into an immunotherapeutic design. The co-potentiation principle may be applicable to other receptors that could be regulated by otherwise inert compounds whose latent potency is only invoked in concert with specific physiologic ligands. äCo-potentiation of antigen recognition: A mechanism to boost weak T ce(epmc).pdf DeepDyve Pubget Overpricing