Fig 3.tif (232.73 kB)
Type I IFN signaling is indispensable for IFN-γ, IL-12 and CXCL10 induction in K. pneumoniae-infected lungs.
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posted on 2017-11-07, 18:24 authored by Masa Ivin, Amy Dumigan, Filipe N. de Vasconcelos, Florian Ebner, Martina Borroni, Anoop Kavirayani, Kornelia N. Przybyszewska, Rebecca J. Ingram, Stefan Lienenklaus, Ulrich Kalinke, Dagmar Stoiber, Jose A. Bengoechea, Pavel KovarikWT and Ifnar1-/- mice were infected intranasally (5 x 104 CFU of K. pneumoniae) for 12 (A, B) or 48 (C) h, or treated with PBS, and gene expression was determined by qPCR normalized to Hprt. (A) Mx1, Ifit1 and Isg15 mRNA levels in lungs. (B, C) Ifng, Il12b, Cxcl10, Tnf and Il10 mRNA levels in lungs. Statistical evaluation: unpaired Student’s t test; error bars, mean ± SEM (n > 3); *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.
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Natural killer cell-intrinsic typeNK cell IFN -γIFN -γ productionNK cell-intrinsic typeIFN receptor 1Ifnar 1NK cell-derived IFN -γ productionalveolar macrophagespneumoniae clearanceCXCLIFN -γ activationlung infection Klebsiella pneumoniaecontrols Klebsiella pneumoniae growthNK cell response-amplifying IL -12exogenous IFN -γ
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