Fig. 7
TNFRI206–211 selectively inhibits TNF-induced activation of p38. In these studies. TNF or FMLF was incubated with TNFRI206–211, then added to cells and examined for activation of MAP kinases and NF-κB (details are given in 'Methods'). a A representative western blot of three experiments shows that TNFRI206–211 but not the scrambled (Sc) TNFR206–211 inhibits TNF-induced p38 activation in human neutrophils and b, c show the quantitative data (mean ± s.e.m. of three experiments) from western blots of the inhibition of TNF-induced p38 activation in neutrophils and MonoMac 6 cells by TNFRI206–211. d The effects of TNFRI206–211 on FMLF-induced p38 activation in neutrophils (n = 3 experiments). e TNFRI206–211 inhibits p38 activation in WEHI cells in response to mouse TNF, which had been pre-treated with TNFR206–211. Results are presented as mean ± s.e.m. of three experiments. TNFR206–211 does not inhibit TNF-induced ERK1/ERK2 activation (f) (n = 3 experiments), JNK (g) (n = 5 experiments) and IκB-α degradation (h) (n = 3 experiments). i TNFR206–211 does not inhibit TNF binding to its receptor (TNFR1) (n = 4 experiments). Quantitated data are mean ± s.e.m. Significance of difference was analysed by one-way ANOVA with either Kruskal–Wallis test followed by Dunn’s multiple comparison test (b, c) or Brown–Forsythe testing followed by Dunnett’s multiple comparison test (d, e, f, g, h) or unpaired Student’s t test (i). *p < 0.05, **p < 0.01 and ***p < 0.001. n.s. not significant
