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10.1002/1521-4141(200103)31:3<726::aid-immu726>3.0.co;2-5 3.0.co;2-5 target="_blank">http://scihub22266oqcxt.onion/10.1002/1521-4141(200103)31:3<726::aid-immu726>3.0.co;2-5 11241276!ä!11241276 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 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       Eur+J+Immunol 2001 ; 31 (3): 726-33 Nephropedia Template TP {{tp|p=11241276|t=2001. Virus infection induces proteolytic processing of IL-18 in human macrophages via caspase-1 and caspase-3 activation |pdf=|usr=}}{{11241276}} gab.com Text Virus infection induces proteolytic processing of IL-18 in human macrophages via caspase-1 and caspase-3 activation JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=11241276 #FOAvip There is increasing evidence that IL-18 is a key pro-inflammatory cytokine and an important mediator of Th1 immune response. The main source of IL-18 is macrophage-like cells. In the present study we have investigated IL-18 protein expression in primary human macrophages in response to influenza A and Sendai virus infections. Macrophages constitutively expressed proIL-18 but produced biologically active IL-18 only after virus infection. The IL-18 release was due to virus infection-induced proteolytic processing of 24-kDa proIL-18 into its mature 18-kDa form. ProIL-18 processing required active caspase-1 enzyme and the release of mature IL-18 was blocked with a caspase-1-specific inhibitor. Caspase-3 inhibitor also reduced IL-18 production in response to virus infection. Inactive proforms of caspase-1 and caspase-3 were basally expressed in macrophages, and virus infection induced the cleavage of procaspases into their mature forms. Besides increasing the expression of caspase proteins, virus infection enhanced caspase mRNA expression in macrophages. The enhancement of caspase gene expression was abrogated by anti-IFN-alpha antibody. Furthermore, IFN-alpha and IFN-gamma could induce caspase gene expression. These results imply that interferons are involved in virus-induced caspase activation that leads to proIL-18 processing and subsequent release of mature IL-18. Twit Text FOAVip Virus infection induces proteolytic processing of IL-18 in human macrophages via caspase-1 and caspase-3 activation ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=11241276 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=11241276 #FOAvip English Wikipedia <ref>{{Cite pmid|11241276}}</ref> Virus infection induces proteolytic processing of IL-18 in human macrophages via caspase-1 and caspase-3 activation #MMPMID11241276 Pirhonen J; Sareneva T; Julkunen I; Matikainen S Eur J Immunol 2001[Mar]; 31 (3): 726-33 PMID11241276show ga There is increasing evidence that IL-18 is a key pro-inflammatory cytokine and an important mediator of Th1 immune response. The main source of IL-18 is macrophage-like cells. In the present study we have investigated IL-18 protein expression in primary human macrophages in response to influenza A and Sendai virus infections. Macrophages constitutively expressed proIL-18 but produced biologically active IL-18 only after virus infection. The IL-18 release was due to virus infection-induced proteolytic processing of 24-kDa proIL-18 into its mature 18-kDa form. ProIL-18 processing required active caspase-1 enzyme and the release of mature IL-18 was blocked with a caspase-1-specific inhibitor. Caspase-3 inhibitor also reduced IL-18 production in response to virus infection. Inactive proforms of caspase-1 and caspase-3 were basally expressed in macrophages, and virus infection induced the cleavage of procaspases into their mature forms. Besides increasing the expression of caspase proteins, virus infection enhanced caspase mRNA expression in macrophages. The enhancement of caspase gene expression was abrogated by anti-IFN-alpha antibody. Furthermore, IFN-alpha and IFN-gamma could induce caspase gene expression. These results imply that interferons are involved in virus-induced caspase activation that leads to proIL-18 processing and subsequent release of mature IL-18. |Caspase 1/genetics/*metabolism[MESH] |Caspase 3[MESH] |Caspase 8[MESH] |Caspase 9[MESH] |Caspases/genetics/*metabolism[MESH] |Cells, Cultured[MESH] |Cysteine Proteinase Inhibitors/pharmacology[MESH] |Enzyme Activation[MESH] |Humans[MESH] |Influenza A virus[MESH] |Interferon-alpha/biosynthesis/physiology[MESH] |Interleukin-1/metabolism[MESH] |Interleukin-18/*metabolism[MESH] |Macrophages/drug effects/metabolism/*virology[MESH] |Oligopeptides/pharmacology[MESH] |Protein Precursors/metabolism[MESH] |RNA, Messenger/biosynthesis[MESH] |Respirovirus[MESH]Virus infection induces proteolytic processing of IL-18 in human macro(epmc).pdf DeepDyve Pubget Overpricing