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10.18632/oncotarget.13978 http://scihub22266oqcxt.onion/10.18632/oncotarget.13978 C5354873!5354873 !28002798     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28002798 &cmd=llinks): Failed to open stream: HTTP request failed! 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IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice |pdf=|usr=}}{{28002798 }} gab.com Text IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28002798 #FOAvip Myeloid-derived suppressor cells (MDSCs) weaken the antitumor immune response through the inhibition of effector T cell activity and the production of immunosuppressive factors in pathological sites. It is well established that interleukin-17A (IL-17A) has a remarkable role on the promotion of inflammation and tumor formation, and IL-17 has been implicated in the enhancement of immunosuppression of MDSCs, which consequently promotes tumor progression. A detailed study of this relationship remains elusive. In our study, we not only confirmed the promotion of IL-17 on Lewis lung carcinoma (LLC) development but also surprisingly showed that IL-17 could extend the fate and enhance the immunosuppressive effect of MDSCs through activating ERK1/2. Additionally, the effect of IL-17 on MDSCs was reversed, even in tumors by blocking ERK1/2. Interdicting the signaling molecule ERK1/2 could increase the apoptosis of MDSCs and weaken the suppressive activity of MDSCs, so that thereafter, the antitumor immunity could be restored partly. Therefore, these findings offer new insights into the importance of IL-17 and the downstream signaling factor ERK1/2 for MDSCs. Twit Text FOAVip IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28002798 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28002798 #FOAvip English Wikipedia <ref>{{Cite pmid|28002798 }}</ref> IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice #MMPMID28002798 Wang J ; Zhang Y ; Yin K ; Xu P ; Tian J ; Ma J ; Tian X ; Wang Y ; Tang X ; Xu H ; Wang S Oncotarget 2017[Jan]; 8 (3 ): 4814-4825 PMID28002798 show ga Myeloid-derived suppressor cells (MDSCs) weaken the antitumor immune response through the inhibition of effector T cell activity and the production of immunosuppressive factors in pathological sites. It is well established that interleukin-17A (IL-17A) has a remarkable role on the promotion of inflammation and tumor formation, and IL-17 has been implicated in the enhancement of immunosuppression of MDSCs, which consequently promotes tumor progression. A detailed study of this relationship remains elusive. In our study, we not only confirmed the promotion of IL-17 on Lewis lung carcinoma (LLC) development but also surprisingly showed that IL-17 could extend the fate and enhance the immunosuppressive effect of MDSCs through activating ERK1/2. Additionally, the effect of IL-17 on MDSCs was reversed, even in tumors by blocking ERK1/2. Interdicting the signaling molecule ERK1/2 could increase the apoptosis of MDSCs and weaken the suppressive activity of MDSCs, so that thereafter, the antitumor immunity could be restored partly. Therefore, these findings offer new insights into the importance of IL-17 and the downstream signaling factor ERK1/2 for MDSCs. |Animals [MESH] |Apoptosis/drug effects [MESH] |Carcinoma, Lewis Lung/immunology/*pathology [MESH] |Cell Line, Tumor [MESH] |Injections, Subcutaneous [MESH] |Interleukin-17/*administration & dosage/pharmacology [MESH] |MAP Kinase Signaling System [MESH] |Mice [MESH]IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs (epmc).pdf DeepDyve Pubget Overpricing