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10.1371/journal.ppat.1006585 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1006585 C5595348!5595348 !28854257     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28854257 &cmd=llinks): Failed to open stream: HTTP request failed! 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HRS plays an important role for TLR7 signaling to orchestrate inflammation and innate immunity upon EV71 infection |pdf=|usr=}}{{28854257 }} gab.com Text HRS plays an important role for TLR7 signaling to orchestrate inflammation and innate immunity upon EV71 infection JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28854257 #FOAvip Enterovirus 71 (EV71) is an RNA virus that causes hand-foot-mouth disease (HFMD), and even fatal encephalitis in children. Although EV71 pathogenesis remains largely obscure, host immune responses may play important roles in the development of diseases. Recognition of pathogens mediated by Toll-like receptors (TLRs) induces host immune and inflammatory responses. Intracellular TLRs must traffic from the endoplasmic reticulum (ER) to the endolysosomal network from where they initiate complete signaling, leading to inflammatory response. This study reveals a novel mechanism underlying the regulation of TLR7 signaling during EV71 infection. Initially, we show that multiple cytokines are differentially expressed during viral infection and demonstrate that EV71 infection induces the production of proinflammatory cytokines through regulating TLR7-mediated p38 MAPK, and NF-?B signaling pathways. Further studies reveal that the expression of the endosome-associated protein hepatocyte growth factor-regulated tyrosine kinase substrate (HRS) is upregulated and highly correlated with the expression of TLR7 in EV71 infected patients, mice, and cultured cells. Virus-induced HRS subsequently enhances TLR7 complex formation in early- and late-endosome by interacting with TLR7 and TAB1. Moreover, HRS is involved in the regulation of the TLR7/NF-?B/p38 MAPK and the TLR7/NF-?B/IRF3 signaling pathways to induce proinflammatory cytokines and interferons, respectively, resulting in the orchestration of inflammatory and immune responses to the EV71 infection. Therefore, this study demonstrates that HRS acts as a key component of TLR7 signaling to orchestrate immune and inflammatory responses during EV71 infection, and provides new insights into the mechanisms underlying the regulation of host inflammation and innate immunity during EV71 infection. Twit Text FOAVip HRS plays an important role for TLR7 signaling to orchestrate inflammation and innate immunity upon EV71 infection ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28854257 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28854257 #FOAvip English Wikipedia <ref>{{Cite pmid|28854257 }}</ref> HRS plays an important role for TLR7 signaling to orchestrate inflammation and innate immunity upon EV71 infection #MMPMID28854257 Luo Z ; Ge M ; Chen J ; Geng Q ; Tian M ; Qiao Z ; Bai L ; Zhang Q ; Zhu C ; Xiong Y ; Wu K ; Liu F ; Liu Y ; Wu J PLoS Pathog 2017[Aug]; 13 (8 ): e1006585 PMID28854257 show ga Enterovirus 71 (EV71) is an RNA virus that causes hand-foot-mouth disease (HFMD), and even fatal encephalitis in children. Although EV71 pathogenesis remains largely obscure, host immune responses may play important roles in the development of diseases. Recognition of pathogens mediated by Toll-like receptors (TLRs) induces host immune and inflammatory responses. Intracellular TLRs must traffic from the endoplasmic reticulum (ER) to the endolysosomal network from where they initiate complete signaling, leading to inflammatory response. This study reveals a novel mechanism underlying the regulation of TLR7 signaling during EV71 infection. Initially, we show that multiple cytokines are differentially expressed during viral infection and demonstrate that EV71 infection induces the production of proinflammatory cytokines through regulating TLR7-mediated p38 MAPK, and NF-?B signaling pathways. Further studies reveal that the expression of the endosome-associated protein hepatocyte growth factor-regulated tyrosine kinase substrate (HRS) is upregulated and highly correlated with the expression of TLR7 in EV71 infected patients, mice, and cultured cells. Virus-induced HRS subsequently enhances TLR7 complex formation in early- and late-endosome by interacting with TLR7 and TAB1. Moreover, HRS is involved in the regulation of the TLR7/NF-?B/p38 MAPK and the TLR7/NF-?B/IRF3 signaling pathways to induce proinflammatory cytokines and interferons, respectively, resulting in the orchestration of inflammatory and immune responses to the EV71 infection. Therefore, this study demonstrates that HRS acts as a key component of TLR7 signaling to orchestrate immune and inflammatory responses during EV71 infection, and provides new insights into the mechanisms underlying the regulation of host inflammation and innate immunity during EV71 infection. |Animals [MESH] |Coxsackievirus Infections/*immunology [MESH] |Endosomal Sorting Complexes Required for Transport/*immunology/metabolism [MESH] |Enterovirus A, Human/*immunology [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Flow Cytometry [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Immunity, Innate/*immunology [MESH] |Immunoblotting [MESH] |Immunoprecipitation [MESH] |Inflammation/*immunology/metabolism [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Microscopy, Fluorescence [MESH] |Phosphoproteins/*immunology/metabolism [MESH] |Polymerase Chain Reaction [MESH]HRS plays an important role for TLR7 signaling to orchestrate inflamma(epmc).pdf DeepDyve Pubget Overpricing