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10.1084/jem.20070891 http://scihub22266oqcxt.onion/10.1084/jem.20070891 C2271005!2271005!18227219     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Exp+Med 2008 ; 205 (2): 323-9 Nephropedia Template TP {{tp|p=18227219|t=2008. Sustained desensitization to bacterial Toll-like receptor ligands after resolutionof respiratory influenza infection |pdf=|usr=}}{{18227219}} gab.com Text Sustained desensitization to bacterial Toll-like receptor ligands after resolutionof respiratory influenza infection JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=18227219 #FOAvip The World Health Organization estimates that lower respiratory tract infections (excluding tuberculosis) account for ?35% of all deaths caused by infectious diseases. In many cases, the cause of death may be caused by multiple pathogens, e.g., the life-threatening bacterial pneumonia observed in patients infected with influenza virus. The ability to evolve more efficient immunity on each successive encounter with antigen is the hallmark of the adaptive immune response. However, in the absence of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the next for extended periods of time. We now report for the first time that this phenomenon is mediated by a sustained desensitization of lung sentinel cells to Toll-like receptor (TLR) ligands; this is an effect that lasts for several months after resolution of influenza or respiratory syncytial virus infection and is associated with reduced chemokine production and NF-?B activation in alveolar macrophages. Although such desensitization may be beneficial in alleviating overall immunopathology, the reduced neutrophil recruitment correlates with heightened bacterial load during secondary respiratory infection. Our data therefore suggests that post-viral desensitization to TLR signals may be one possible contributor to the common secondary bacterial pneumonia associated with pandemic and seasonal influenza infection. Twit Text FOAVip Sustained desensitization to bacterial Toll-like receptor ligands after resolutionof respiratory influenza infection ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=18227219 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18227219 #FOAvip English Wikipedia <ref>{{Cite pmid|18227219}}</ref> Sustained desensitization to bacterial Toll-like receptor ligands after resolutionof respiratory influenza infection #MMPMID18227219 Didierlaurent A; Goulding J; Patel S; Snelgrove R; Low L; Bebien M; Lawrence T; van Rijt LS; Lambrecht BN; Sirard JC; Hussell T J Exp Med 2008[Feb]; 205 (2): 323-9 PMID18227219show ga The World Health Organization estimates that lower respiratory tract infections (excluding tuberculosis) account for ?35% of all deaths caused by infectious diseases. In many cases, the cause of death may be caused by multiple pathogens, e.g., the life-threatening bacterial pneumonia observed in patients infected with influenza virus. The ability to evolve more efficient immunity on each successive encounter with antigen is the hallmark of the adaptive immune response. However, in the absence of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the next for extended periods of time. We now report for the first time that this phenomenon is mediated by a sustained desensitization of lung sentinel cells to Toll-like receptor (TLR) ligands; this is an effect that lasts for several months after resolution of influenza or respiratory syncytial virus infection and is associated with reduced chemokine production and NF-?B activation in alveolar macrophages. Although such desensitization may be beneficial in alleviating overall immunopathology, the reduced neutrophil recruitment correlates with heightened bacterial load during secondary respiratory infection. Our data therefore suggests that post-viral desensitization to TLR signals may be one possible contributor to the common secondary bacterial pneumonia associated with pandemic and seasonal influenza infection. äSustained desensitization to bacterial Toll-like receptor ligands afte(epmc).pdf DeepDyve Pubget Overpricing