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10.4049/jimmunol.1302729 http://scihub22266oqcxt.onion/10.4049/jimmunol.1302729 C4048787!4048787!24790150     free     free     free 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 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 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2014 ; 192 (12): 5839-51 Nephropedia Template TP {{tp|p=24790150|t=2014. Soluble, but not transmembrane, TNF-? is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology |pdf=|usr=}}{{24790150}} gab.com Text Soluble, but not transmembrane, TNF- is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24790150 #FOAvip TNF-? is a pleotropic cytokine, which has both proinflammatory and anti-inflammatory functions during influenza infection. TNF-? is first expressed as a transmembrane (mem) protein that is proteolytically processed to release a soluble (sol) form. memTNF-? and solTNF-? have been shown to exert distinct tissue-protective or -pathologic effects in several disease models. However, the relative contributions of memTNF-? or solTNF-? in regulating pulmonary immunopathology following influenza infection are unclear. Therefore, we performed intranasal influenza infection in mice exclusively expressing non-cleavable memTNF-? or lacking TNF-? entirely and examined the outcomes. We found that solTNF-?, but not memTNF-?, was required to limit the size of the immune response and the extent of injury. In the absence of solTNF-?, there was a significant increase in the CD8+ T-cell response, including virus-specific CD8+ T-cells, which was due in part to an increased resistance to activation-induced cell death. We found that solTNF-? mediates these immunoregulatory effects primarily through TNF receptor 1 (TNFR1), since mice deficient in TNFR1, but not TNFR2, exhibited dysregulated immune responses and exacerbated injury similar to that observed in mice lacking solTNF-?. We also found that solTNF-? expression was required early during infection to regulate the magnitude of the CD8+ T-cell response indicating that early inflammatory events are critical for the regulation of the effector phase. Taken together, these findings suggest that processing of memTNF-? to release solTNF-? is a critical event regulating the immune response during influenza infection. Twit Text FOAVip Soluble, but not transmembrane, TNF- is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24790150 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24790150 #FOAvip English Wikipedia <ref>{{Cite pmid|24790150}}</ref> Soluble, but not transmembrane, TNF-? is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology #MMPMID24790150 DeBerge MP; Ely KH; Enelow RI J Immunol 2014[Jun]; 192 (12): 5839-51 PMID24790150show ga TNF-? is a pleotropic cytokine, which has both proinflammatory and anti-inflammatory functions during influenza infection. TNF-? is first expressed as a transmembrane (mem) protein that is proteolytically processed to release a soluble (sol) form. memTNF-? and solTNF-? have been shown to exert distinct tissue-protective or -pathologic effects in several disease models. However, the relative contributions of memTNF-? or solTNF-? in regulating pulmonary immunopathology following influenza infection are unclear. Therefore, we performed intranasal influenza infection in mice exclusively expressing non-cleavable memTNF-? or lacking TNF-? entirely and examined the outcomes. We found that solTNF-?, but not memTNF-?, was required to limit the size of the immune response and the extent of injury. In the absence of solTNF-?, there was a significant increase in the CD8+ T-cell response, including virus-specific CD8+ T-cells, which was due in part to an increased resistance to activation-induced cell death. We found that solTNF-? mediates these immunoregulatory effects primarily through TNF receptor 1 (TNFR1), since mice deficient in TNFR1, but not TNFR2, exhibited dysregulated immune responses and exacerbated injury similar to that observed in mice lacking solTNF-?. We also found that solTNF-? expression was required early during infection to regulate the magnitude of the CD8+ T-cell response indicating that early inflammatory events are critical for the regulation of the effector phase. Taken together, these findings suggest that processing of memTNF-? to release solTNF-? is a critical event regulating the immune response during influenza infection. äSoluble, but not transmembrane, TNF-? is required during influenza inf(epmc).pdf DeepDyve Pubget Overpricing