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10.1038/ncomms10554 http://scihub22266oqcxt.onion/10.1038/ncomms10554 C4749981!4749981!26861112     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       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=26861112|t=2016. NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions |pdf=|usr=}}{{26861112}} gab.com Text NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26861112 #FOAvip NLRC5 is a transcriptional regulator of MHC class I (MHCI), which maintains high MHCI expression particularly in T cells. Recent evidence highlights an important NK?T-cell crosstalk, raising the question on whether NLRC5 specifically modulates this interaction. Here we show that NK cells from Nlrc5-deficient mice exhibit moderate alterations in inhibitory receptor expression and responsiveness. Interestingly, NLRC5 expression in T cells is required to protect them from NK-cell-mediated elimination upon inflammation. Using T-cell-specific Nlrc5-deficient mice, we show that NK cells surprisingly break tolerance even towards ?self' Nlrc5-deficient T cells under inflammatory conditions. Furthermore, during chronic LCMV infection, the total CD8+ T-cell population is severely decreased in these mice, a phenotype reverted by NK-cell depletion. These findings strongly suggest that endogenous T cells with low MHCI expression become NK-cell targets, having thus important implications for T-cell responses in naturally or therapeutically induced inflammatory conditions. Twit Text FOAVip NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26861112 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26861112 #FOAvip English Wikipedia <ref>{{Cite pmid|26861112}}</ref> NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions #MMPMID26861112 Ludigs K; Jandus C; Utzschneider DT; Staehli F; Bessoles S; Dang AT; Rota G; Castro W; Zehn D; Vivier E; Held W; Romero P; Guarda G Nat Commun 2016[]; 7 (ä): ä PMID26861112show ga NLRC5 is a transcriptional regulator of MHC class I (MHCI), which maintains high MHCI expression particularly in T cells. Recent evidence highlights an important NK?T-cell crosstalk, raising the question on whether NLRC5 specifically modulates this interaction. Here we show that NK cells from Nlrc5-deficient mice exhibit moderate alterations in inhibitory receptor expression and responsiveness. Interestingly, NLRC5 expression in T cells is required to protect them from NK-cell-mediated elimination upon inflammation. Using T-cell-specific Nlrc5-deficient mice, we show that NK cells surprisingly break tolerance even towards ?self' Nlrc5-deficient T cells under inflammatory conditions. Furthermore, during chronic LCMV infection, the total CD8+ T-cell population is severely decreased in these mice, a phenotype reverted by NK-cell depletion. These findings strongly suggest that endogenous T cells with low MHCI expression become NK-cell targets, having thus important implications for T-cell responses in naturally or therapeutically induced inflammatory conditions. äNLRC5 shields T lymphocytes from NK-cell-mediated elimination under in(epmc).pdf DeepDyve Pubget Overpricing