Skip to main content
Fig. 6 | Respiratory Research

Fig. 6

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

Fig. 6

Induction of IFNγ by endogenous IL-18 required the IL-18-producing cells to be in close proximity to NK cells. IFNγ release was induced by stimulating either PBMC with IL-12 and LPS (a) or by stimulating NK cells with IL-12, LPS and monocytes in a co-culture system (b) or segregating NK and monocytes in a transwell system (c). IFNγ production by NK cells was determined in the presence of Anakinra (IL-1 antagonist), IL-18BP (IL-18 antagonist), or a control IgG1. 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 and median from n = 5 donors (a) and n = 4 donors (b-c). p’ values calculated with Friedman test with Dunn’s multiple comparison test (d) Bright field micrograph exemplifying the typical and common close proximity of IL-18+ cells (Vina green chromogen) and CD56+ cells (brown DAB) in a lung section. Scale bar denotes 18 μm

Back to article page