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10.1038/s41467-018-04376-5 http://scihub22266oqcxt.onion/10.1038/s41467-018-04376-5 C5964249!5964249!29789522     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=29789522|t=2018. A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation |pdf=|usr=}}{{29789522}} gab.com Text A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29789522 #FOAvip Microglia, the mononuclear phagocytes of the central nervous system (CNS), are important for the maintenance of CNS homeostasis, but also critically contribute to CNS pathology. Here we demonstrate that the nuclear factor kappa B (NF-?B) regulatory protein A20 is crucial in regulating microglia activation during CNS homeostasis and pathology. In mice, deletion of A20 in microglia increases microglial cell number and affects microglial regulation of neuronal synaptic function. Administration of a sublethal dose of lipopolysaccharide induces massive microglia activation, neuroinflammation, and lethality in mice with microglia-confined A20 deficiency. Microglia A20 deficiency also exacerbates multiple sclerosis (MS)-like disease, due to hyperactivation of the Nlrp3 inflammasome leading to enhanced interleukin-1? secretion and CNS inflammation. Finally, we confirm a Nlrp3 inflammasome signature and IL-1? expression in brain and cerebrospinal fluid from MS patients. Collectively, these data reveal a critical role for A20 in the control of microglia activation and neuroinflammation. Twit Text FOAVip A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29789522 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29789522 #FOAvip English Wikipedia <ref>{{Cite pmid|29789522}}</ref> A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation #MMPMID29789522 Voet S; Mc Guire C; Hagemeyer N; Martens A; Schroeder A; Wieghofer P; Daems C; Staszewski O; Vande Walle L; Jordao MJC; Sze M; Vikkula HK; Demeestere D; Van Imschoot G; Scott CL; Hoste E; Gonçalves A; Guilliams M; Lippens S; Libert C; Vandenbroucke RE; Kim KW; Jung S; Callaerts-Vegh Z; Callaerts P; de Wit J; Lamkanfi M; Prinz M; van Loo G Nat Commun 2018[]; 9 (ä): ä PMID29789522show ga Microglia, the mononuclear phagocytes of the central nervous system (CNS), are important for the maintenance of CNS homeostasis, but also critically contribute to CNS pathology. Here we demonstrate that the nuclear factor kappa B (NF-?B) regulatory protein A20 is crucial in regulating microglia activation during CNS homeostasis and pathology. In mice, deletion of A20 in microglia increases microglial cell number and affects microglial regulation of neuronal synaptic function. Administration of a sublethal dose of lipopolysaccharide induces massive microglia activation, neuroinflammation, and lethality in mice with microglia-confined A20 deficiency. Microglia A20 deficiency also exacerbates multiple sclerosis (MS)-like disease, due to hyperactivation of the Nlrp3 inflammasome leading to enhanced interleukin-1? secretion and CNS inflammation. Finally, we confirm a Nlrp3 inflammasome signature and IL-1? expression in brain and cerebrospinal fluid from MS patients. Collectively, these data reveal a critical role for A20 in the control of microglia activation and neuroinflammation. äA20 critically controls microglia activation and inhibits inflammasome(epmc).pdf DeepDyve Pubget Overpricing