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An interferon-β-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage.

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Title: An interferon-β-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage.
Authors: Inoue, Makoto, Chen, Po-han, Siecinski, Stephen, Li, Qi-jing, Liu, Chunlei, Steinman, Lawrence, Gregory, Simon G, Benner, Eric, Shinohara, Mari L
Source: Nature Neuroscience. Dec2016, Vol. 19 Issue 12, p1599-1609. 11p. 7 Graphs.
Abstract: Inflammation induced by innate immunity influences the development of T cell-mediated autoimmunity in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). We found that strong activation of innate immunity induced Nod-like receptor protein 3 (NLRP3) inflammasome-independent and interferon-β (IFNβ)-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate immunity requires the NLRP3 inflammasome and is sensitive to IFNβ treatment. Instead, an alternative inflammatory mechanism, including membrane-bound lymphotoxin-β receptor (LTβR) and CXC chemokine receptor 2 (CXCR2), is involved in type B EAE development, and type B EAE is ameliorated by antagonizing these receptors. Relative expression of Ltbr and Cxcr2 genes was indeed enhanced in patients with IFNβ-resistant multiple sclerosis. Remission was minimal in type B EAE due to neuronal damages induced by semaphorin 6B upregulation on CD4+ T cells. Our data reveal a new inflammatory mechanism by which an IFNβ-resistant EAE subtype develops. [ABSTRACT FROM AUTHOR]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: An interferon-β-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage.
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  Data: <searchLink fieldCode="AR" term="%22Inoue%2C+Makoto%22">Inoue, Makoto</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Po-han%22">Chen, Po-han</searchLink><br /><searchLink fieldCode="AR" term="%22Siecinski%2C+Stephen%22">Siecinski, Stephen</searchLink><br /><searchLink fieldCode="AR" term="%22Li%2C+Qi-jing%22">Li, Qi-jing</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Chunlei%22">Liu, Chunlei</searchLink><br /><searchLink fieldCode="AR" term="%22Steinman%2C+Lawrence%22">Steinman, Lawrence</searchLink><br /><searchLink fieldCode="AR" term="%22Gregory%2C+Simon+G%22">Gregory, Simon G</searchLink><br /><searchLink fieldCode="AR" term="%22Benner%2C+Eric%22">Benner, Eric</searchLink><br /><searchLink fieldCode="AR" term="%22Shinohara%2C+Mari+L%22">Shinohara, Mari L</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Nature+Neuroscience%22">Nature Neuroscience</searchLink>. Dec2016, Vol. 19 Issue 12, p1599-1609. 11p. 7 Graphs.
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  Label: Abstract
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  Data: Inflammation induced by innate immunity influences the development of T cell-mediated autoimmunity in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). We found that strong activation of innate immunity induced Nod-like receptor protein 3 (NLRP3) inflammasome-independent and interferon-β (IFNβ)-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate immunity requires the NLRP3 inflammasome and is sensitive to IFNβ treatment. Instead, an alternative inflammatory mechanism, including membrane-bound lymphotoxin-β receptor (LTβR) and CXC chemokine receptor 2 (CXCR2), is involved in type B EAE development, and type B EAE is ameliorated by antagonizing these receptors. Relative expression of Ltbr and Cxcr2 genes was indeed enhanced in patients with IFNβ-resistant multiple sclerosis. Remission was minimal in type B EAE due to neuronal damages induced by semaphorin 6B upregulation on CD4+ T cells. Our data reveal a new inflammatory mechanism by which an IFNβ-resistant EAE subtype develops. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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