Signal transduction analysis of the NLRP3-inflammasome pathway after cellular damage and its paracrine regulation

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• 作者：Denise Veltman^a ; Thessa Laeremans^a ; Egle Passante^b ; Heinrich J. Huber^a ; ^c ; ¹ ; ^{heinrich.huber@ovgu.de}
• 关键词：Signal transduction modelling ; NLRP3-Inflammasome ; Interferons ; Inflammatory diseases ; Ordinary Differential Equations
• 刊名：Journal of Theoretical Biology
• 出版年：2017
• 出版时间：21 February 2017
• 年：2017
• 卷：415
• 期：Complete
• 页码：125-136
• 全文大小：943 K
• 卷排序：415

文摘

We provide a pathway model of the NLRP3-inflammasome after cellular damage. NLRP3-inflammasome attenuation by paracrine IFN-I is more potent than by IFN-II. Change from IFN-II to IFN-I may stop inflammation during tissue repair after infarct. Impairment of IFN-I feedback can lead to hyperinflammation as in spontaneous colitis. Regulation of inflammation may directly be encoded within regulatory pathways.