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10.1513/AnnalsATS.201403-105AW http://scihub22266oqcxt.onion/10.1513/AnnalsATS.201403-105AW C4298970!4298970 !25525732     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25525732 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Ann+Am+Thorac+Soc 2014 ; 11 Suppl 5 (Suppl 5 ): S277-83 Nephropedia Template TP {{tp|p=25525732 |t=2014. Airway fibrinogenolysis and the initiation of allergic inflammation |pdf=|usr=}}{{25525732 }} gab.com Text Airway fibrinogenolysis and the initiation of allergic inflammation JO: Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=25525732 #FOAvip The past 15 years of allergic disease research have produced extraordinary improvements in our understanding of the pathogenesis of airway allergic diseases such as asthma. Whereas it was previously viewed as largely an immunoglobulin E-mediated process, the gradual recognition that T cells, especially Type 2 T helper (Th2) cells and Th17 cells, play a major role in asthma and related afflictions has inspired clinical trials targeting cytokine-based inflammatory pathways that show great promise. What has yet to be clarified about the pathogenesis of allergic inflammatory disorders, however, are the fundamental initiating factors, both exogenous and endogenous, that drive and sustain B- and T-cell responses that underlie the expression of chronic disease. Here we review how proteinases derived from diverse sources drive allergic responses. A central discovery supporting the proteinase hypothesis of allergic disease pathophysiology is the role played by airway fibrinogen, which in part appears to serve as a sensor of unregulated proteinase activity and which, when cleaved, both participates in a novel allergic signaling pathway through Toll-like receptor 4 and forms fibrin clots that contribute to airway obstruction. Unresolved at present is the ultimate source of airway allergenic proteinases. From among many potential candidates, perhaps the most intriguing is the possibility such enzymes derive from airway fungi. Together, these new findings expand both our knowledge of allergic disease pathophysiology and options for therapeutic intervention. Twit Text FOAVip Airway fibrinogenolysis and the initiation of allergic inflammation ????Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=25525732 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25525732 #FOAvip English Wikipedia <ref>{{Cite pmid|25525732 }}</ref> Airway fibrinogenolysis and the initiation of allergic inflammation #MMPMID25525732 Millien VO ; Lu W ; Mak G ; Yuan X ; Knight JM ; Porter P ; Kheradmand F ; Corry DB Ann Am Thorac Soc 2014[Dec]; 11 Suppl 5 (Suppl 5 ): S277-83 PMID25525732 show ga The past 15 years of allergic disease research have produced extraordinary improvements in our understanding of the pathogenesis of airway allergic diseases such as asthma. Whereas it was previously viewed as largely an immunoglobulin E-mediated process, the gradual recognition that T cells, especially Type 2 T helper (Th2) cells and Th17 cells, play a major role in asthma and related afflictions has inspired clinical trials targeting cytokine-based inflammatory pathways that show great promise. What has yet to be clarified about the pathogenesis of allergic inflammatory disorders, however, are the fundamental initiating factors, both exogenous and endogenous, that drive and sustain B- and T-cell responses that underlie the expression of chronic disease. Here we review how proteinases derived from diverse sources drive allergic responses. A central discovery supporting the proteinase hypothesis of allergic disease pathophysiology is the role played by airway fibrinogen, which in part appears to serve as a sensor of unregulated proteinase activity and which, when cleaved, both participates in a novel allergic signaling pathway through Toll-like receptor 4 and forms fibrin clots that contribute to airway obstruction. Unresolved at present is the ultimate source of airway allergenic proteinases. From among many potential candidates, perhaps the most intriguing is the possibility such enzymes derive from airway fungi. Together, these new findings expand both our knowledge of allergic disease pathophysiology and options for therapeutic intervention. |*Immunity, Cellular [MESH] |Allergens/*immunology [MESH] |Asthma/*immunology/metabolism [MESH] |Cytokines/*metabolism [MESH] |Fibrinogen/*metabolism [MESH] |Humans [MESH] |Hypersensitivity/*immunology/metabolism [MESH] |Inflammation/*immunology/metabolism [MESH] |Respiratory System/immunology [MESH]Airway fibrinogenolysis and the initiation of allergic inflammation (epmc).pdf DeepDyve Pubget Overpricing