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10.1016/j.celrep.2017.02.079 http://scihub22266oqcxt.onion/10.1016/j.celrep.2017.02.079 C5379012!5379012!28329691     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2017 ; 18 (12): 3005-17 Nephropedia Template TP {{tp|p=28329691|t=2017. Myocardial Infarction Primes Autoreactive T Cells through Activation of Dendritic Cells |pdf=|usr=}}{{28329691}} gab.com Text Myocardial Infarction Primes Autoreactive T Cells through Activation of Dendritic Cells JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=28329691 #FOAvip Peripheral tolerance is crucial for avoiding activation of self-reactive T cells to tissue-restricted antigens. Sterile tissue injury can break peripheral tolerance, but it is unclear how autoreactive T cells get activated in response to self. An example of a sterile injury is myocardial infarction (MI). We hypothesized that tissue necrosis is an activator of dendritic cells (DCs), which control tolerance to self-antigens. DC subsets of a murine healthy heart consisted of IRF8-dependent conventional (c)DC1, IRF4-dependent cDC2, and monocyte-derived DCs. In steady state, cardiac self-antigen ?-myosin was presented in the heart-draining mediastinal lymph node (mLN) by cDC1s, driving the proliferation of antigen-specific CD4+ TCR-M T cells and their differentiation into regulatory cells (Tregs). Following MI, all DC subsets infiltrated the heart, whereas only cDCs migrated to the mLN. Here, cDC2s induced TCR-M proliferation and differentiation into interleukin-(IL)-17/interferon-(IFN)?-producing effector cells. Thus, cardiac-specific autoreactive T cells get activated by mature DCs following myocardial infarction. Twit Text FOAVip Myocardial Infarction Primes Autoreactive T Cells through Activation of Dendritic Cells ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=28329691 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28329691 #FOAvip English Wikipedia <ref>{{Cite pmid|28329691}}</ref> Myocardial Infarction Primes Autoreactive T Cells through Activation of Dendritic Cells #MMPMID28329691 Van der Borght K; Scott CL; Nindl V; Bouché A; Martens L; Sichien D; Van Moorleghem J; Vanheerswynghels M; De Prijck S; Saeys Y; Ludewig B; Gillebert T; Guilliams M; Carmeliet P; Lambrecht BN Cell Rep 2017[Mar]; 18 (12): 3005-17 PMID28329691show ga Peripheral tolerance is crucial for avoiding activation of self-reactive T cells to tissue-restricted antigens. Sterile tissue injury can break peripheral tolerance, but it is unclear how autoreactive T cells get activated in response to self. An example of a sterile injury is myocardial infarction (MI). We hypothesized that tissue necrosis is an activator of dendritic cells (DCs), which control tolerance to self-antigens. DC subsets of a murine healthy heart consisted of IRF8-dependent conventional (c)DC1, IRF4-dependent cDC2, and monocyte-derived DCs. In steady state, cardiac self-antigen ?-myosin was presented in the heart-draining mediastinal lymph node (mLN) by cDC1s, driving the proliferation of antigen-specific CD4+ TCR-M T cells and their differentiation into regulatory cells (Tregs). Following MI, all DC subsets infiltrated the heart, whereas only cDCs migrated to the mLN. Here, cDC2s induced TCR-M proliferation and differentiation into interleukin-(IL)-17/interferon-(IFN)?-producing effector cells. Thus, cardiac-specific autoreactive T cells get activated by mature DCs following myocardial infarction. äMyocardial Infarction Primes Autoreactive T Cells through Activation o(epmc).pdf DeepDyve Pubget Overpricing