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http://scihub22266oqcxt.onion/ 10358182!ä!10358182 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 1999 ; 162 (12): 7322-9 Nephropedia Template TP {{tp|p=10358182|t=1999. Virus infection activates IL-1 beta and IL-18 production in human macrophages by a caspase-1-dependent pathway |pdf=|usr=}}{{10358182}} gab.com Text Virus infection activates IL-1 beta and IL-18 production in human macrophages by a caspase-1-dependent pathway JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=10358182 #FOAvip Monocytes and macrophages play a significant role in host's defense system, since they produce a number of cytokines in response to microbial infections. We have studied IL-1 beta, IL-18, IFN-alpha/beta, and TNF-alpha gene expression and protein production in human primary monocytes and GM-CSF-differentiated macrophages during influenza A and Sendai virus infections. Virus-infected monocytes released only small amounts of IL-1 beta or IL-18 protein, whereas 7- and 14-day-old GM-CSF-differentiated macrophages readily produced these cytokines. Constitutive expression of proIL-18 was seen in monocytes and macrophages, and the expression of it was enhanced during monocyte/macrophage differentiation. Expression of IL-18 mRNA was clearly induced only by Sendai virus, whereas both influenza A and Sendai viruses induced IL-1 beta mRNA expression. Since caspase-1 is known to cleave proIL-1 beta and proIL-18 into their mature, active forms, we analyzed the effect of a specific caspase-1 inhibitor on virus-induced IL-1 beta and IL-18 production. The release of IL-1 beta and IL-18, but not that of IFN-alpha/beta or TNF-alpha, was clearly blocked by the inhibitor. Our results suggest that the cellular differentiation is a crucial factor that affects the capacity of monocytes/macrophages to produce IL-1 beta and IL-18 in response to virus infections. Furthermore, the virus-induced activation of caspase-1 is required for the efficient production of biologically active IL-1 beta and IL-18. Twit Text FOAVip Virus infection activates IL-1 beta and IL-18 production in human macrophages by a caspase-1-dependent pathway ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=10358182 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=10358182 #FOAvip English Wikipedia <ref>{{Cite pmid|10358182}}</ref> Virus infection activates IL-1 beta and IL-18 production in human macrophages by a caspase-1-dependent pathway #MMPMID10358182 Pirhonen J; Sareneva T; Kurimoto M; Julkunen I; Matikainen S J Immunol 1999[Jun]; 162 (12): 7322-9 PMID10358182show ga Monocytes and macrophages play a significant role in host's defense system, since they produce a number of cytokines in response to microbial infections. We have studied IL-1 beta, IL-18, IFN-alpha/beta, and TNF-alpha gene expression and protein production in human primary monocytes and GM-CSF-differentiated macrophages during influenza A and Sendai virus infections. Virus-infected monocytes released only small amounts of IL-1 beta or IL-18 protein, whereas 7- and 14-day-old GM-CSF-differentiated macrophages readily produced these cytokines. Constitutive expression of proIL-18 was seen in monocytes and macrophages, and the expression of it was enhanced during monocyte/macrophage differentiation. Expression of IL-18 mRNA was clearly induced only by Sendai virus, whereas both influenza A and Sendai viruses induced IL-1 beta mRNA expression. Since caspase-1 is known to cleave proIL-1 beta and proIL-18 into their mature, active forms, we analyzed the effect of a specific caspase-1 inhibitor on virus-induced IL-1 beta and IL-18 production. The release of IL-1 beta and IL-18, but not that of IFN-alpha/beta or TNF-alpha, was clearly blocked by the inhibitor. Our results suggest that the cellular differentiation is a crucial factor that affects the capacity of monocytes/macrophages to produce IL-1 beta and IL-18 in response to virus infections. Furthermore, the virus-induced activation of caspase-1 is required for the efficient production of biologically active IL-1 beta and IL-18. |Caspase 1/genetics/*physiology[MESH] |Cell Differentiation/drug effects/immunology[MESH] |Cell-Free System/physiology[MESH] |Cells, Cultured[MESH] |Gene Expression Regulation/drug effects/immunology[MESH] |Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology[MESH] |Humans[MESH] |Influenza A virus/*immunology[MESH] |Interferon-gamma/biosynthesis[MESH] |Interleukin-1/*biosynthesis/genetics/metabolism[MESH] |Interleukin-18/*biosynthesis/genetics/metabolism/physiology[MESH] |Kinetics[MESH] |Macrophage Activation/*immunology[MESH] |Macrophages/enzymology/*immunology/metabolism/virology[MESH] |Monocytes/cytology/enzymology/metabolism/virology[MESH] |Protein Precursors/biosynthesis[MESH] |Signal Transduction/immunology[MESH]Virus infection activates IL-1 beta and IL-18 production in human macr(epmc).pdf DeepDyve Pubget Overpricing