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. Author manuscript; available in PMC: 2014 Dec 23.
Published in final edited form as: J Autoimmun. 2011 Mar 16;36(0):263–277. doi: 10.1016/j.jaut.2011.02.005

Fig. 10. The T cell cytokine profile shifts from IL-17F toward IFN-γ production under the influence of IL-18.

Fig. 10

(A) NOD and IL-18KO NOD splenocytes were cultured with anti-CD3/CD28 and brefeldin A for 5 hours (n=8 spleens/strain). Alternatively, LPS (50 µg /mouse, i.v.) was administered to NOD (n=4) and IL-18KO NOD (n=3) mice and splenocytes were harvested 3 hours later and cultured with brefeldin A for an additional 3 h. Flow cytometry was used to measure the percentages of IFN-γ+ CD44high cells (delineated by the boxed regions). (B) Comparison of IL-17F expression by CD4+ cells that were activated in vitro with anti-CD3/CD28. The histogram shows isotype control staining (shaded) and IL-17F staining in NOD (thin line) and IL-18KO NOD (bold line) cells. These results are representative of 8 mice/strain. (C) BDC2.5 NOD splenocytes were injected into NODScid mice along with daily injections of PBS or IL-18 (n=3 mice/group). Four days later, the spleens were harvested and the lymphocytes were cultured with anti-CD3/CD28 for analysis of IL-17F and IFN-γ expression in Vβ4+ CD62Llow/− cells. This experiment was repeated twice with similar results. (*) denotes a statistically significant difference between NOD and IL-18KO NOD mice or PBS and IL-18 treatment groups for the indicated T cell population.