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10.1016/j.immuni.2020.01.006 http://scihub22266oqcxt.onion/10.1016/j.immuni.2020.01.006 32049050!ä!32049050 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunity 2020 ; 52 (2): 328-341.e5 Nephropedia Template TP {{tp|p=32049050|t=2020. Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells |pdf=|usr=}}{{32049050}} gab.com Text Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=32049050 #FOAvip Fever, an evolutionarily conserved physiological response to infection, is also commonly associated with many autoimmune diseases, but its role in T cell differentiation and autoimmunity remains largely unclear. T helper 17 (Th17) cells are critical in host defense and autoinflammatory diseases, with distinct phenotypes and pathogenicity. Here, we show that febrile temperature selectively regulated Th17 cell differentiation in vitro in enhancing interleukin-17 (IL-17), IL-17F, and IL-22 expression. Th17 cells generated under febrile temperature (38.5 degrees C-39.5 degrees C), compared with those under 37 degrees C, showed enhanced pathogenic gene expression with increased pro-inflammatory activities in vivo. Mechanistically, febrile temperature promoted SUMOylation of SMAD4 transcription factor to facilitate its nuclear localization; SMAD4 deficiency selectively abrogated the effects of febrile temperature on Th17 cell differentiation both in vitro and ameliorated an autoimmune disease model. Our results thus demonstrate a critical role of fever in shaping adaptive immune responses with implications in autoimmune diseases. Twit Text FOAVip Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=32049050 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32049050 #FOAvip English Wikipedia <ref>{{Cite pmid|32049050}}</ref> Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells #MMPMID32049050 Wang X; Ni L; Wan S; Zhao X; Ding X; Dejean A; Dong C Immunity 2020[Feb]; 52 (2): 328-341.e5 PMID32049050show ga Fever, an evolutionarily conserved physiological response to infection, is also commonly associated with many autoimmune diseases, but its role in T cell differentiation and autoimmunity remains largely unclear. T helper 17 (Th17) cells are critical in host defense and autoinflammatory diseases, with distinct phenotypes and pathogenicity. Here, we show that febrile temperature selectively regulated Th17 cell differentiation in vitro in enhancing interleukin-17 (IL-17), IL-17F, and IL-22 expression. Th17 cells generated under febrile temperature (38.5 degrees C-39.5 degrees C), compared with those under 37 degrees C, showed enhanced pathogenic gene expression with increased pro-inflammatory activities in vivo. Mechanistically, febrile temperature promoted SUMOylation of SMAD4 transcription factor to facilitate its nuclear localization; SMAD4 deficiency selectively abrogated the effects of febrile temperature on Th17 cell differentiation both in vitro and ameliorated an autoimmune disease model. Our results thus demonstrate a critical role of fever in shaping adaptive immune responses with implications in autoimmune diseases. |Adaptive Immunity[MESH] |Animals[MESH] |Body Temperature/*immunology[MESH] |Cell Differentiation/immunology[MESH] |Cell Nucleus/metabolism[MESH] |Cytokines/metabolism[MESH] |Encephalomyelitis, Autoimmune, Experimental/genetics/immunology[MESH] |Fever/genetics/*immunology[MESH] |Gene Expression Regulation[MESH] |Heat-Shock Response/immunology[MESH] |Mice[MESH] |Smad4 Protein/deficiency/metabolism[MESH] |Sumoylation[MESH]Febrile Temperature Critically Controls the Differentiation and Pathog(epmc).pdf DeepDyve Pubget Overpricing