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10.1186/s12974-017-0899-1 http://scihub22266oqcxt.onion/10.1186/s12974-017-0899-1 C5483301!5483301!28646890     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Neuroinflammation 2017 ; 14 (ä): ä Nephropedia Template TP {{tp|p=28646890|t=2017. Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination |pdf=|usr=}}{{28646890}} gab.com Text Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination JO: J Neuroinflammation http://www.kidney.de/pget.php?&tw=1&pmid=28646890 #FOAvip Background: Antibodies with specificity for myelin oligodendrocyte glycoprotein (MOG) are implicated in multiple sclerosis and related diseases. The pathogenic importance of anti-MOG antibody in primary demyelinating pathology remains poorly characterized. Objective: The objective of this study is to investigate whether administration of anti-MOG antibody would be sufficient for demyelination and to determine if type I interferon (IFN) signaling plays a similar role in anti-MOG antibody-mediated pathology, as has been shown for neuromyelitis optica-like pathology. Methods: Purified IgG2a monoclonal anti-MOG antibody and mouse complement were stereotactically injected into the corpus callosum of wild-type and type I IFN receptor deficient mice (IFNAR1-KO) with and without pre-established experimental autoimmune encephalomyelitis (EAE). Results: Anti-MOG induced complement-dependent demyelination in the corpus callosum of wild-type mice and did not occur in mice that received control IgG2a. Deposition of activated complement coincided with demyelination, and this was significantly reduced in IFNAR1-KO mice. Co-injection of anti-MOG and complement at onset of symptoms of EAE induced similar levels of callosal demyelination in wild-type and IFNAR1-KO mice. Conclusions: Anti-MOG antibody and complement was sufficient to induce callosal demyelination, and pathology was dependent on type I IFN. Induction of EAE in IFNAR1-KO mice overcame the dependence on type I IFN for anti-MOG and complement-mediated demyelination. Electronic supplementary material: The online version of this article (doi:10.1186/s12974-017-0899-1) contains supplementary material, which is available to authorized users. Twit Text FOAVip Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination ????J Neuroinflammation http://www.kidney.de/pget.php?&tw=1&pmid=28646890 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28646890 #FOAvip English Wikipedia <ref>{{Cite pmid|28646890}}</ref> Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination #MMPMID28646890 Berg CT; Khorooshi R; Asgari N; Owens T J Neuroinflammation 2017[]; 14 (ä): ä PMID28646890show ga Background: Antibodies with specificity for myelin oligodendrocyte glycoprotein (MOG) are implicated in multiple sclerosis and related diseases. The pathogenic importance of anti-MOG antibody in primary demyelinating pathology remains poorly characterized. Objective: The objective of this study is to investigate whether administration of anti-MOG antibody would be sufficient for demyelination and to determine if type I interferon (IFN) signaling plays a similar role in anti-MOG antibody-mediated pathology, as has been shown for neuromyelitis optica-like pathology. Methods: Purified IgG2a monoclonal anti-MOG antibody and mouse complement were stereotactically injected into the corpus callosum of wild-type and type I IFN receptor deficient mice (IFNAR1-KO) with and without pre-established experimental autoimmune encephalomyelitis (EAE). Results: Anti-MOG induced complement-dependent demyelination in the corpus callosum of wild-type mice and did not occur in mice that received control IgG2a. Deposition of activated complement coincided with demyelination, and this was significantly reduced in IFNAR1-KO mice. Co-injection of anti-MOG and complement at onset of symptoms of EAE induced similar levels of callosal demyelination in wild-type and IFNAR1-KO mice. Conclusions: Anti-MOG antibody and complement was sufficient to induce callosal demyelination, and pathology was dependent on type I IFN. Induction of EAE in IFNAR1-KO mice overcame the dependence on type I IFN for anti-MOG and complement-mediated demyelination. Electronic supplementary material: The online version of this article (doi:10.1186/s12974-017-0899-1) contains supplementary material, which is available to authorized users. äInfluence of type I IFN signaling on anti-MOG antibody-mediated demyel(epmc).pdf DeepDyve Pubget Overpricing