Figure 3
IFN-γ deficiency exacerbated the inflammatory response. (A) IL-17 expression in splenocytes from WT and IFN-γ-knockout mice incubated for 3 days under Th17 cell-polarizing conditions (stimulation only with anti-CD3 and anti-CD28 with TGF-β and IL-6) was measured by flow cytometry (n = 6). (B) IL-17 and TNF-α expression was analysed by ELISA using splenocytes from WT and IFN-γ-knockout mice cultured for 72 hours under Th17 cell-polarizing conditions (n = 6). (C) and (D) Relative mRNA expression was analysed by real-time PCR using splenocytes from WT and IFN-γ-knockout mice treated with TNF-α for 1 hour. (E) The level of p-STAT3 is expressed as a relative ratio and t-STAT3 was used to normalize the data. Splenocytes from WT and IFN-γ-knockout mice were stimulated under Th17-polarizing conditions. The cells were then prepared for determination of p-STAT3 and t-STAT3 expression. Data are expressed as mean ± standard deviation (SD) of three independent experiments (**P < 0.01, ***P < 0.005).
