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10.1128/CMR.00090-16 http://scihub22266oqcxt.onion/10.1128/CMR.00090-16 C5355638!5355638!28179378     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Microbiol+Rev 2017 ; 30 (2): 481-502 Nephropedia Template TP {{tp|p=28179378|t=2017. The Human Immune Response to Respiratory Syncytial Virus Infection |pdf=|usr=}}{{28179378}} gab.com Text The Human Immune Response to Respiratory Syncytial Virus Infection JO: Clin Microbiol Rev http://www.kidney.de/pget.php?&tw=1&pmid=28179378 #FOAvip Respiratory syncytial virus (RSV) is an important etiological agent of respiratory infections, particularly in children. Much information regarding the immune response to RSV comes from animal models and in vitro studies. Here, we provide a comprehensive description of the human immune response to RSV infection, based on a systematic literature review of research on infected humans. There is an initial strong neutrophil response to RSV infection in humans, which is positively correlated with disease severity and mediated by interleukin-8 (IL-8). Dendritic cells migrate to the lungs as the primary antigen-presenting cell. An initial systemic T-cell lymphopenia is followed by a pulmonary CD8+ T-cell response, mediating viral clearance. Humoral immunity to reinfection is incomplete, but RSV IgG and IgA are protective. B-cell-stimulating factors derived from airway epithelium play a major role in protective antibody generation. Gamma interferon (IFN-?) has a strongly protective role, and a Th2-biased response may be deleterious. Other cytokines (particularly IL-17A), chemokines (particularly CCL-5 and CCL-3), and local innate immune factors (including cathelicidins and IFN-?) contribute to pathogenesis. In summary, neutrophilic inflammation is incriminated as a harmful response, whereas CD8+ T cells and IFN-? have protective roles. These may represent important therapeutic targets to modulate the immunopathogenesis of RSV infection. Twit Text FOAVip The Human Immune Response to Respiratory Syncytial Virus Infection ????Clin Microbiol Rev http://www.kidney.de/pget.php?&tw=1&pmid=28179378 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28179378 #FOAvip English Wikipedia <ref>{{Cite pmid|28179378}}</ref> The Human Immune Response to Respiratory Syncytial Virus Infection #MMPMID28179378 Russell CD; Unger SA; Walton M; Schwarze J Clin Microbiol Rev 2017[Apr]; 30 (2): 481-502 PMID28179378show ga Respiratory syncytial virus (RSV) is an important etiological agent of respiratory infections, particularly in children. Much information regarding the immune response to RSV comes from animal models and in vitro studies. Here, we provide a comprehensive description of the human immune response to RSV infection, based on a systematic literature review of research on infected humans. There is an initial strong neutrophil response to RSV infection in humans, which is positively correlated with disease severity and mediated by interleukin-8 (IL-8). Dendritic cells migrate to the lungs as the primary antigen-presenting cell. An initial systemic T-cell lymphopenia is followed by a pulmonary CD8+ T-cell response, mediating viral clearance. Humoral immunity to reinfection is incomplete, but RSV IgG and IgA are protective. B-cell-stimulating factors derived from airway epithelium play a major role in protective antibody generation. Gamma interferon (IFN-?) has a strongly protective role, and a Th2-biased response may be deleterious. Other cytokines (particularly IL-17A), chemokines (particularly CCL-5 and CCL-3), and local innate immune factors (including cathelicidins and IFN-?) contribute to pathogenesis. In summary, neutrophilic inflammation is incriminated as a harmful response, whereas CD8+ T cells and IFN-? have protective roles. These may represent important therapeutic targets to modulate the immunopathogenesis of RSV infection. äThe Human Immune Response to Respiratory Syncytial Virus Infection (epmc).pdf DeepDyve Pubget Overpricing