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. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Eur J Immunol. 2015 Aug 28;45(11):3052–3063. doi: 10.1002/eji.201545696

Figure 4. IL-33 deficiency leads to reduced NK-cell IFN-γ production during acute viral hepatitis.

Figure 4

WT and IL-33−/− mice were infected, and then sacrificed at 3 dpi. (A) The percentage of liver NK cells was determined by gating on CD3- NK1.1+ populations. (B) IHLs were isolated and stimulated with PMA and Ionomycin for 5 hours in the presence of GolgiStop, followed by intracellular staining of IFN-γ. The percentages of IFN-γ-producing NK cells are shown. Serum IFN-γ levels at 3 and 6 dpi are shown. (C) Granzyme B staining of NK cells (solid gray is isotype control; solid line is WT NK cell and dash line is IL-33−/− NK cells. (D) Cells from LN of naïve WT mice were cultured with rIL-33 (10 ng/ml) in the presence of rIL-7 (20 ng/ml) for 4 days. Cells were stimulated with PMA and Ionomycin in the presence of GolgiStop during the last 5 hours, and intracellular IFN-γ and IL-17 were detected. The data are shown as mean + SEM of n = 3–5 mice/group from single experiments representative of at least three experiments performed. A two-tailed t test was used for comparison between two groups. *P<0.05,***P<0.001.