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10.1016/j.jid.2016.06.618 http://scihub22266oqcxt.onion/10.1016/j.jid.2016.06.618 C5070969!5070969 !27388993     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27388993 &cmd=llinks): Failed to open stream: HTTP request failed! 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AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production |pdf=|usr=}}{{27388993 }} gab.com Text AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production JO: J Invest Dermatol http://www.kidney.de/pget.php?&tw=1&pmid=27388993 #FOAvip Prominent skin involvement is a defining characteristic of autoinflammatory disorders caused by abnormal IL-1 signaling. However, the pathways and cell types that drive cutaneous autoinflammatory features remain poorly understood. We sought to address this issue by investigating the pathogenesis of pustular psoriasis, a model of autoinflammatory disorders with predominant cutaneous manifestations. We specifically characterized the impact of mutations affecting AP1S3, a disease gene previously identified by our group and validated here in a newly ascertained patient resource. We first showed that AP1S3 expression is distinctively elevated in keratinocytes. Because AP1S3 encodes a protein implicated in autophagosome formation, we next investigated the effects of gene silencing on this pathway. We found that AP1S3 knockout disrupts keratinocyte autophagy, causing abnormal accumulation of p62, an adaptor protein mediating NF-?B activation. We showed that as a consequence, AP1S3-deficient cells up-regulate IL-1 signaling and overexpress IL-36?, a cytokine that is emerging as an important mediator of skin inflammation. These abnormal immune profiles were recapitulated by pharmacological inhibition of autophagy and verified in patient keratinocytes, where they were reversed by IL-36 blockade. These findings show that keratinocytes play a key role in skin autoinflammation and identify autophagy modulation of IL-36 signaling as a therapeutic target. Twit Text FOAVip AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production ????J Invest Dermatol http://www.kidney.de/pget.php?&tw=1&pmid=27388993 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27388993 #FOAvip English Wikipedia <ref>{{Cite pmid|27388993 }}</ref> AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production #MMPMID27388993 Mahil SK ; Twelves S ; Farkas K ; Setta-Kaffetzi N ; Burden AD ; Gach JE ; Irvine AD ; Képíró L ; Mockenhaupt M ; Oon HH ; Pinner J ; Ranki A ; Seyger MMB ; Soler-Palacin P ; Storan ER ; Tan ES ; Valeyrie-Allanore L ; Young HS ; Trembath RC ; Choon SE ; Szell M ; Bata-Csorgo Z ; Smith CH ; Di Meglio P ; Barker JN ; Capon F J Invest Dermatol 2016[Nov]; 136 (11 ): 2251-2259 PMID27388993 show ga Prominent skin involvement is a defining characteristic of autoinflammatory disorders caused by abnormal IL-1 signaling. However, the pathways and cell types that drive cutaneous autoinflammatory features remain poorly understood. We sought to address this issue by investigating the pathogenesis of pustular psoriasis, a model of autoinflammatory disorders with predominant cutaneous manifestations. We specifically characterized the impact of mutations affecting AP1S3, a disease gene previously identified by our group and validated here in a newly ascertained patient resource. We first showed that AP1S3 expression is distinctively elevated in keratinocytes. Because AP1S3 encodes a protein implicated in autophagosome formation, we next investigated the effects of gene silencing on this pathway. We found that AP1S3 knockout disrupts keratinocyte autophagy, causing abnormal accumulation of p62, an adaptor protein mediating NF-?B activation. We showed that as a consequence, AP1S3-deficient cells up-regulate IL-1 signaling and overexpress IL-36?, a cytokine that is emerging as an important mediator of skin inflammation. These abnormal immune profiles were recapitulated by pharmacological inhibition of autophagy and verified in patient keratinocytes, where they were reversed by IL-36 blockade. These findings show that keratinocytes play a key role in skin autoinflammation and identify autophagy modulation of IL-36 signaling as a therapeutic target. |*Mutation [MESH] |*Up-Regulation [MESH] |Adaptor Proteins, Signal Transducing/*genetics/metabolism [MESH] |Aged [MESH] |Autophagy [MESH] |Cell Line [MESH] |DNA Mutational Analysis [MESH] |DNA/*genetics [MESH] |Female [MESH] |Humans [MESH] |Interleukin-1/*biosynthesis/genetics [MESH] |Keratinocytes/*metabolism/pathology [MESH] |Middle Aged [MESH] |Psoriasis/*genetics/metabolism/pathology [MESH] |Signal Transduction [MESH]AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte(epmc).pdf DeepDyve Pubget Overpricing