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10.1016/j.jaut.2020.102508 http://scihub22266oqcxt.onion/10.1016/j.jaut.2020.102508 32624353!7332282!32624353     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Autoimmun 2020 ; 114 (ä): 102508 Nephropedia Template TP {{tp|p=32624353|t=2020. Prostaglandin D2 signaling in dendritic cells is critical for the development of EAE |pdf=|usr=}}{{32624353}} gab.com Text Prostaglandin D2 signaling in dendritic cells is critical for the development of EAE JO: J Autoimmun http://www.kidney.de/pget.php?&tw=1&pmid=32624353 #FOAvip Priming of autoreactive T cells in lymph nodes by dendritic cells (DCs) is critical for the pathogenesis of experimental autoimmune encephalitis (EAE). DC activation reflects a balance of pro- and anti-inflammatory signals. One anti-inflammatory factor is prostaglandin D2 signaling through its cognate receptor, D-prostanoid receptor 1 (PTGDR), on myeloid cells. Loss of PTGDR signaling might be expected to enhance DC activation and EAE but here we show that PTGDR(-/)(-) mice developed only mild signs of MOG(35-55) peptide immunization-induced EAE. Compared to wild type mice, PTGDR(-/)(-) mice exhibited less demyelination, decreased leukocyte infiltration and diminished microglia activation. These effects resulted from increased pro-inflammatory responses in the lymph nodes, most notably in IL-1beta production, with the unexpected consequence of increased activation-induced apoptosis of MOG(35-55) peptide-specific T cells. Conditional deletion of PTGDR on DCs, and not other myeloid cells ameliorated EAE. Together, these results demonstrate the indispensable role that PGD(2)/PTGDR signaling on DCs has in development of pathogenic T cells in autoimmune demyelination. Twit Text FOAVip Prostaglandin D2 signaling in dendritic cells is critical for the development of EAE ????J Autoimmun http://www.kidney.de/pget.php?&tw=1&pmid=32624353 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32624353 #FOAvip English Wikipedia <ref>{{Cite pmid|32624353}}</ref> Prostaglandin D2 signaling in dendritic cells is critical for the development of EAE #MMPMID32624353 Zheng J; Sariol A; Meyerholz D; Zhang Q; Abrahante Llorens JE; Narumiya S; Perlman S J Autoimmun 2020[Nov]; 114 (ä): 102508 PMID32624353show ga Priming of autoreactive T cells in lymph nodes by dendritic cells (DCs) is critical for the pathogenesis of experimental autoimmune encephalitis (EAE). DC activation reflects a balance of pro- and anti-inflammatory signals. One anti-inflammatory factor is prostaglandin D2 signaling through its cognate receptor, D-prostanoid receptor 1 (PTGDR), on myeloid cells. Loss of PTGDR signaling might be expected to enhance DC activation and EAE but here we show that PTGDR(-/)(-) mice developed only mild signs of MOG(35-55) peptide immunization-induced EAE. Compared to wild type mice, PTGDR(-/)(-) mice exhibited less demyelination, decreased leukocyte infiltration and diminished microglia activation. These effects resulted from increased pro-inflammatory responses in the lymph nodes, most notably in IL-1beta production, with the unexpected consequence of increased activation-induced apoptosis of MOG(35-55) peptide-specific T cells. Conditional deletion of PTGDR on DCs, and not other myeloid cells ameliorated EAE. Together, these results demonstrate the indispensable role that PGD(2)/PTGDR signaling on DCs has in development of pathogenic T cells in autoimmune demyelination. |*Disease Susceptibility[MESH] |*Signal Transduction[MESH] |Adoptive Transfer/methods[MESH] |Animals[MESH] |B7-H1 Antigen/metabolism[MESH] |Biomarkers[MESH] |Dendritic Cells/*immunology/*metabolism[MESH] |Disease Models, Animal[MESH] |Encephalomyelitis, Autoimmune, Experimental/*etiology/*metabolism/pathology/therapy[MESH] |Lymphocyte Activation/genetics/immunology[MESH] |Lymphocyte Count[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Programmed Cell Death 1 Receptor/metabolism[MESH] |Prostaglandin D2/*metabolism[MESH] |Receptors, Immunologic/genetics/metabolism[MESH] |Receptors, Prostaglandin/genetics/metabolism[MESH] |T-Cell Antigen Receptor Specificity[MESH]Prostaglandin D2 signaling in dendritic cells is critical for the deve(epmc).pdf DeepDyve Pubget Overpricing