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10.1172/JCI133115 http://scihub22266oqcxt.onion/10.1172/JCI133115 31710309!6877329!31710309     free     free     free       J+Clin+Invest 2019 ; 129 (12): 5086-5088 Nephropedia Template TP {{tp|p=31710309|t=2019. Destress and do not suppress: targeting adrenergic signaling in tumor immunosuppression |pdf=|usr=}}{{31710309}} gab.com Text Destress and do not suppress: targeting adrenergic signaling in tumor immunosuppression JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=31710309 #FOAvip Tumor-induced immunosuppression is a common obstacle for cancer treatment. Adrenergic signaling triggered by chronic stress participates in the creation of an immunosuppressive microenvironment by promoting myeloid-derived suppressor cell (MDSC) proliferation and activation. In this issue of the JCI, Mohammadpour et al. elegantly delve into the mechanisms underlying MDSC contribution to tumor development. They used in vitro and in vivo mouse models to demonstrate that chronic stress results in MDSC accumulation, survival, and immune-inhibitory activity. Of therapeutic relevance, the authors showed that propranolol, a commonly prescribed beta-blocker, can reduce MDSC immunosuppression and enhance the effect of other cancer therapies. Twit Text FOAVip Destress and do not suppress: targeting adrenergic signaling in tumor immunosuppression ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=31710309 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31710309 #FOAvip English Wikipedia <ref>{{Cite pmid|31710309}}</ref> Destress and do not suppress: targeting adrenergic signaling in tumor immunosuppression #MMPMID31710309 Inigo-Marco I; Alonso MM J Clin Invest 2019[Dec]; 129 (12): 5086-5088 PMID31710309show ga Tumor-induced immunosuppression is a common obstacle for cancer treatment. Adrenergic signaling triggered by chronic stress participates in the creation of an immunosuppressive microenvironment by promoting myeloid-derived suppressor cell (MDSC) proliferation and activation. In this issue of the JCI, Mohammadpour et al. elegantly delve into the mechanisms underlying MDSC contribution to tumor development. They used in vitro and in vivo mouse models to demonstrate that chronic stress results in MDSC accumulation, survival, and immune-inhibitory activity. Of therapeutic relevance, the authors showed that propranolol, a commonly prescribed beta-blocker, can reduce MDSC immunosuppression and enhance the effect of other cancer therapies. |*Neoplasms[MESH] |Adrenergic Agents[MESH] |Animals[MESH] |Immunosuppression Therapy[MESH] |Mice[MESH] |Myeloid Cells/immunology[MESH] |Myeloid-Derived Suppressor Cells/*immunology[MESH] |Receptors, Adrenergic, beta-2[MESH]Destress and do not suppress: targeting adrenergic signaling in tumor (epmc).pdf DeepDyve Pubget Overpricing