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10.4049/jimmunol.1400722 http://scihub22266oqcxt.onion/10.4049/jimmunol.1400722 C4053538!4053538!24813205     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24813205&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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2014 ; 192 (12): 5490-8 Nephropedia Template TP {{tp|p=24813205|t=2014. Antigen-dependent versus -independent activation of iNKT cells during infection |pdf=|usr=}}{{24813205}} gab.com Text Antigen-dependent versus -independent activation of iNKT cells during infection JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24813205 #FOAvip CD1d-reactive invariant natural killer T cells (iNKT) play a vital role in determining the characteristics of immune responses to infectious agents. Previous reports suggest that iNKT cell activation during infection can be: 1) solely driven by cytokines from innate immune cells; 2) require microbial-antigen; or 3) require self-antigen. In this study, we examined the role of antigen receptor stimulation in iNKT cells during several bacterial and viral infections. To test for antigen receptor signaling, Nur77gfp BAC transgenic mice, which upregulate GFP in response to antigen receptor but not inflammatory signals, were analyzed. iNKT cells in the reporter mice infected with mouse cytomegalovirus (MCMV) produced IFN? but did not upregulate GFP, consistent with their reported CD1d-independent activation. However, two bacteria known to produce lipid antigens for iNKT cells induced GFP expression and cytokine production. In contrast, although Salmonella typhimurium (S. typhimurium) was proposed to induce the presentation of a self-lipid, iNKT cells produced IFN?, but did not upregulate GFP after infection in vivo. Even in CD1d-deficient hosts, iNKT cells were still able to produce IFN? after S. typhimurium infection. Furthermore, while it has been proposed that endogenous lipid presentation is a result of Toll-like receptor (TLR) stimulation of antigen presenting cells, injection of different TLR agonists led to iNKT cell IFN? but not increased GFP expression. These data indicate that robust iNKT cell responses to bacteria as well as viruses can be obtained in the absence of antigenic stimulation. Twit Text FOAVip Antigen-dependent versus -independent activation of iNKT cells during infection ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24813205 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24813205 #FOAvip English Wikipedia <ref>{{Cite pmid|24813205}}</ref> Antigen-dependent versus -independent activation of iNKT cells during infection #MMPMID24813205 Holzapfel KL; Tyznik AJ; Kronenberg M; Hogquist KA J Immunol 2014[Jun]; 192 (12): 5490-8 PMID24813205show ga CD1d-reactive invariant natural killer T cells (iNKT) play a vital role in determining the characteristics of immune responses to infectious agents. Previous reports suggest that iNKT cell activation during infection can be: 1) solely driven by cytokines from innate immune cells; 2) require microbial-antigen; or 3) require self-antigen. In this study, we examined the role of antigen receptor stimulation in iNKT cells during several bacterial and viral infections. To test for antigen receptor signaling, Nur77gfp BAC transgenic mice, which upregulate GFP in response to antigen receptor but not inflammatory signals, were analyzed. iNKT cells in the reporter mice infected with mouse cytomegalovirus (MCMV) produced IFN? but did not upregulate GFP, consistent with their reported CD1d-independent activation. However, two bacteria known to produce lipid antigens for iNKT cells induced GFP expression and cytokine production. In contrast, although Salmonella typhimurium (S. typhimurium) was proposed to induce the presentation of a self-lipid, iNKT cells produced IFN?, but did not upregulate GFP after infection in vivo. Even in CD1d-deficient hosts, iNKT cells were still able to produce IFN? after S. typhimurium infection. Furthermore, while it has been proposed that endogenous lipid presentation is a result of Toll-like receptor (TLR) stimulation of antigen presenting cells, injection of different TLR agonists led to iNKT cell IFN? but not increased GFP expression. These data indicate that robust iNKT cell responses to bacteria as well as viruses can be obtained in the absence of antigenic stimulation. äAntigen-dependent versus -independent activation of iNKT cells during (epmc).pdf DeepDyve Pubget Overpricing