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http://scihub22266oqcxt.onion/ 7706733!ä!7706733 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 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 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 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 1995 ; 154 (8): 3952-60 Nephropedia Template TP {{tp|p=7706733|t=1995. Neutrophil deactivation by influenza A virus Role of hemagglutinin binding to specific sialic acid-bearing cellular proteins |pdf=|usr=}}{{7706733}} gab.com Text Neutrophil deactivation by influenza A virus Role of hemagglutinin binding to specific sialic acid-bearing cellular proteins JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=7706733 #FOAvip Bacterial superinfections are the most common cause of mortality during influenza epidemics. Depression of phagocyte functions by influenza A viruses (IAVs) is a likely contributory cause of such infections. We used an in vitro model of viral depression of neutrophil respiratory burst responses to FMLP and PMA to examine the mechanism of IAV-induced phagocyte deactivation. Respiratory burst responses or intracellular calcium mobilization were triggered by the virus itself, but these were not causally related to deactivation. By treating neutrophils with neuraminidase, and by use of purified IAV hemagglutinin (HA) preparations, cross-linking of sialic acid-bearing neutrophil surface components by the IAV HA was shown to be responsible for deactivation. IAV competed for binding to neutrophils with Abs directed against CD43, sialyl-Le(x), CD45, and gangliosides. Deactivation could be reproduced by treating neutrophils with anti-CD43 or -sialyl-Le(x) Abs in the absence of IAV. However, treatment of neutrophils with elastase markedly reduced CD43 expression, without affecting overall IAV binding or the ability of IAV to cause deactivation. Hence, although IAV binding to CD43 can account for deactivation, other IAV-binding proteins exist (e.g., those bearing sialyl-Le(x)) that can independently mediate functional depression. Twit Text FOAVip Neutrophil deactivation by influenza A virus Role of hemagglutinin binding to specific sialic acid-bearing cellular proteins ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=7706733 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=7706733 #FOAvip English Wikipedia <ref>{{Cite pmid|7706733}}</ref> Neutrophil deactivation by influenza A virus Role of hemagglutinin binding to specific sialic acid-bearing cellular proteins #MMPMID7706733 Hartshorn KL; Liou LS; White MR; Kazhdan MM; Tauber JL; Tauber AI J Immunol 1995[Apr]; 154 (8): 3952-60 PMID7706733show ga Bacterial superinfections are the most common cause of mortality during influenza epidemics. Depression of phagocyte functions by influenza A viruses (IAVs) is a likely contributory cause of such infections. We used an in vitro model of viral depression of neutrophil respiratory burst responses to FMLP and PMA to examine the mechanism of IAV-induced phagocyte deactivation. Respiratory burst responses or intracellular calcium mobilization were triggered by the virus itself, but these were not causally related to deactivation. By treating neutrophils with neuraminidase, and by use of purified IAV hemagglutinin (HA) preparations, cross-linking of sialic acid-bearing neutrophil surface components by the IAV HA was shown to be responsible for deactivation. IAV competed for binding to neutrophils with Abs directed against CD43, sialyl-Le(x), CD45, and gangliosides. Deactivation could be reproduced by treating neutrophils with anti-CD43 or -sialyl-Le(x) Abs in the absence of IAV. However, treatment of neutrophils with elastase markedly reduced CD43 expression, without affecting overall IAV binding or the ability of IAV to cause deactivation. Hence, although IAV binding to CD43 can account for deactivation, other IAV-binding proteins exist (e.g., those bearing sialyl-Le(x)) that can independently mediate functional depression. |Antigens, CD/metabolism[MESH] |Antigens, Surface/metabolism[MESH] |Calcium/metabolism[MESH] |Concanavalin A/pharmacology[MESH] |Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology[MESH] |Hemagglutinins, Viral/pharmacology[MESH] |Humans[MESH] |Hydrogen Peroxide/metabolism[MESH] |Immunity, Cellular[MESH] |In Vitro Techniques[MESH] |Influenza A virus/*immunology[MESH] |Leukocyte Elastase[MESH] |Macrophage-1 Antigen/metabolism[MESH] |N-Formylmethionine Leucyl-Phenylalanine/pharmacology[MESH] |Neuraminidase/pharmacology[MESH] |Neutrophil Activation[MESH] |Neutrophils/*immunology[MESH] |Pancreatic Elastase/pharmacology[MESH] |Receptors, Virus/metabolism[MESH] |Sialic Acids/physiology[MESH] |Superoxides/metabolism[MESH]Neutrophil deactivation by influenza A virus Role of hemagglutinin bi(epmc).pdf DeepDyve Pubget Overpricing