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10.1038/s41598-017-16147-1 http://scihub22266oqcxt.onion/10.1038/s41598-017-16147-1 C5700082!5700082 !29167489     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29167489 &cmd=llinks): Failed to open stream: HTTP request failed! 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T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure |pdf=|usr=}}{{29167489 }} gab.com Text T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29167489 #FOAvip We investigated whether CD4(+)-T cells with specificity for an antigen in cardiomyocytes promote the progression from hypertrophy to heart failure in mice with increased pressure load due to transverse aortic constriction (TAC). OT-II mice expressing a transgenic T cell receptor (TCR) with specificity for ovalbumin (OVA) on CD4(+)-T cells and cMy-mOVA mice expressing OVA on cardiomyocytes were crossed. The resulting cMy-mOVA-OT-II mice did not display signs of spontaneous autoimmunity despite the fact that their OVA-specific CD4(+)-T cells were not anergic. After TAC, progression to heart failure was significantly accelerated in cMy-mOVA-OT-II compared to cMy-mOVA mice. No OVA-specific antibodies were induced in response to TAC in cMy-mOVA-OT-II mice, yet more CD3(+) T cells infiltrated their myocardium when compared with TAC-operated cMy-mOVA mice. Systemically, the proportion of activated CD4(+)-T cells with a Th(1) and Th(17) cytokine profile was increased in cMy-mOVA-OT-II mice after TAC. Thus, T helper cells with specificity for an antigen in cardiomyocytes can directly promote the progression of heart failure in response to pressure overload independently of autoantibodies. Twit Text FOAVip T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29167489 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29167489 #FOAvip English Wikipedia <ref>{{Cite pmid|29167489 }}</ref> T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure #MMPMID29167489 Gröschel C ; Sasse A ; Röhrborn C ; Monecke S ; Didié M ; Elsner L ; Kruse V ; Bunt G ; Lichtman AH ; Toischer K ; Zimmermann WH ; Hasenfuß G ; Dressel R Sci Rep 2017[Nov]; 7 (1 ): 15998 PMID29167489 show ga We investigated whether CD4(+)-T cells with specificity for an antigen in cardiomyocytes promote the progression from hypertrophy to heart failure in mice with increased pressure load due to transverse aortic constriction (TAC). OT-II mice expressing a transgenic T cell receptor (TCR) with specificity for ovalbumin (OVA) on CD4(+)-T cells and cMy-mOVA mice expressing OVA on cardiomyocytes were crossed. The resulting cMy-mOVA-OT-II mice did not display signs of spontaneous autoimmunity despite the fact that their OVA-specific CD4(+)-T cells were not anergic. After TAC, progression to heart failure was significantly accelerated in cMy-mOVA-OT-II compared to cMy-mOVA mice. No OVA-specific antibodies were induced in response to TAC in cMy-mOVA-OT-II mice, yet more CD3(+) T cells infiltrated their myocardium when compared with TAC-operated cMy-mOVA mice. Systemically, the proportion of activated CD4(+)-T cells with a Th(1) and Th(17) cytokine profile was increased in cMy-mOVA-OT-II mice after TAC. Thus, T helper cells with specificity for an antigen in cardiomyocytes can directly promote the progression of heart failure in response to pressure overload independently of autoantibodies. |Animals [MESH] |CD8-Positive T-Lymphocytes/immunology/metabolism [MESH] |Disease Progression [MESH] |Echocardiography [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Female [MESH] |Heart Failure/immunology/metabolism/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Myocytes, Cardiac/immunology/metabolism/*pathology [MESH] |Ovalbumin/adverse effects [MESH] |Receptors, Antigen, T-Cell/metabolism [MESH]T helper cells with specificity for an antigen in cardiomyocytes promo(epmc).pdf DeepDyve Pubget Overpricing