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10.1073/pnas.1700858114 http://scihub22266oqcxt.onion/10.1073/pnas.1700858114 C5617250!5617250 !28794279     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28794279 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (38 ): 10226-10231 Nephropedia Template TP {{tp|p=28794279 |t=2017. Nasopharyngeal infection by Streptococcus pyogenes requires superantigen-responsive V?-specific T cells |pdf=|usr=}}{{28794279 }} gab.com Text Nasopharyngeal infection by Streptococcus pyogenes requires superantigen-responsive V -specific T cells JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28794279 #FOAvip The globally prominent pathogen Streptococcus pyogenes secretes potent immunomodulatory proteins known as superantigens (SAgs), which engage lateral surfaces of major histocompatibility class II molecules and T-cell receptor (TCR) ?-chain variable domains (V?s). These interactions result in the activation of numerous V?-specific T cells, which is the defining activity of a SAg. Although streptococcal SAgs are known virulence factors in scarlet fever and toxic shock syndrome, mechanisms by how SAgs contribute to the life cycle of S. pyogenes remain poorly understood. Herein, we demonstrate that passive immunization against the V?8-targeting SAg streptococcal pyrogenic exotoxin A (SpeA), or active immunization with either wild-type or a nonfunctional SpeA mutant, protects mice from nasopharyngeal infection; however, only passive immunization, or vaccination with inactive SpeA, resulted in high-titer SpeA-specific antibodies in vivo. Mice vaccinated with wild-type SpeA rendered V?8(+) T cells poorly responsive, which prevented infection. This phenotype was reproduced with staphylococcal enterotoxin B, a heterologous SAg that also targets V?8(+) T cells, and rendered mice resistant to infection. Furthermore, antibody-mediated depletion of T cells prevented nasopharyngeal infection by S. pyogenes, but not by Streptococcus pneumoniae, a bacterium that does not produce SAgs. Remarkably, these observations suggest that S. pyogenes uses SAgs to manipulate V?-specific T cells to establish nasopharyngeal infection. Twit Text FOAVip Nasopharyngeal infection by Streptococcus pyogenes requires superantigen-responsive V -specific T cells ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28794279 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28794279 #FOAvip English Wikipedia <ref>{{Cite pmid|28794279 }}</ref> Nasopharyngeal infection by Streptococcus pyogenes requires superantigen-responsive V?-specific T cells #MMPMID28794279 Zeppa JJ ; Kasper KJ ; Mohorovic I ; Mazzuca DM ; Haeryfar SMM ; McCormick JK Proc Natl Acad Sci U S A 2017[Sep]; 114 (38 ): 10226-10231 PMID28794279 show ga The globally prominent pathogen Streptococcus pyogenes secretes potent immunomodulatory proteins known as superantigens (SAgs), which engage lateral surfaces of major histocompatibility class II molecules and T-cell receptor (TCR) ?-chain variable domains (V?s). These interactions result in the activation of numerous V?-specific T cells, which is the defining activity of a SAg. Although streptococcal SAgs are known virulence factors in scarlet fever and toxic shock syndrome, mechanisms by how SAgs contribute to the life cycle of S. pyogenes remain poorly understood. Herein, we demonstrate that passive immunization against the V?8-targeting SAg streptococcal pyrogenic exotoxin A (SpeA), or active immunization with either wild-type or a nonfunctional SpeA mutant, protects mice from nasopharyngeal infection; however, only passive immunization, or vaccination with inactive SpeA, resulted in high-titer SpeA-specific antibodies in vivo. Mice vaccinated with wild-type SpeA rendered V?8(+) T cells poorly responsive, which prevented infection. This phenotype was reproduced with staphylococcal enterotoxin B, a heterologous SAg that also targets V?8(+) T cells, and rendered mice resistant to infection. Furthermore, antibody-mediated depletion of T cells prevented nasopharyngeal infection by S. pyogenes, but not by Streptococcus pneumoniae, a bacterium that does not produce SAgs. Remarkably, these observations suggest that S. pyogenes uses SAgs to manipulate V?-specific T cells to establish nasopharyngeal infection. ?Nasopharyngeal infection by Streptococcus pyogenes requires superant(epmc).pdf DeepDyve Pubget Overpricing