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Fig. 5 | Respiratory Research

Fig. 5

From: IL-18 associated with lung lymphoid aggregates drives IFNγ production in severe COPD

Fig. 5

Blocking endogenous IL-18 activity did not significantly impact IFNγ release by NK cells stimulated with supernatants of infected NHBE cells or activated monocytes. Human NK cells were incubated for 24 h with supernatants from HRV14-infected NHBE cells (a) or LPS-treated monocytes (b) in the presence of IL-12, a known enhancer of IFNγ production. IFNγ production by NK cells was determined in the presence (+) of Anakinra (IL-1 antagonist), IL-18BP (IL-18 antagonist), a control IgG1 isotype or no addition (−). Due to donor to donor variations in the level of IFNγ response, the mean values across experiments were determined after normalization to IFNγ levels observed in the supernatant of NK cells stimulated in absence of antagonists. Data show the individual data points from independent experiments and the median (n = 2 (a) and n = 3 (b)). Statistical significance was assessed with the Friedman test with Dunn’s multiple comparison test (p’ indicates the adjusted p values)

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