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. 2019 Aug 28;10:3878. doi: 10.1038/s41467-019-11858-7

Fig. 6.

Fig. 6

A pathogenic role of the TNFα-TNFRI axis during T cell-mediated autoinflammation. a Staining of MEFs co-cultured with T cells. Scale bars: 100 μm. Magnified images are shown on the right. bd Percentage of surviving cells in a (b), Sharpin−/− MEFs co-cultured with the indicated T cells (c), and the indicated CRISPR/Cas9-targeted MEFs (d) n = 4 biologically independent experiments. e Treatment with a TNFα-neutralizing antibody or solubilized TNFRII. f Treatment with z-VAD-fmk and/or Nec1. The iCelligence system was used to measure cell viability. g, h Survival after 10 h of the treatment described in f (g) or after siRNA knockdown (h). n = 4 independent experiments. i Expression of the indicated receptors on the T cell surface after TCR stimulation. j Disease progression among the indicated strains. M, Male; F, Female. k Immunofluorescence staining of skin sections. Scale bars: 20 μm. l Ratio of CD3εintTCRβ+:CD3εhiTCRγδ+ cells. n= 6 biologically independent animals. m Number of TCRβ+ T cells in the skin. n= 4 biologically independent animals. n Percentage of TNFα- and/or IFNγ-expressing TCRβ+ T cells in the skin. n = 4 biologically independent animals. o Dot plots representing TRM cells. p, q MFI or percentage of cells expressing the indicated surface proteins. n = 8 biologically independent animals. Small horizontal lines indicate the mean (±s.e.m.). *p < 0.05, **p < 0.01, ***p < 0.001. Kruskal–Wallis test with Bonferroni correction (α value = 0.05) was used for bd, g, and h, while two-tailed Mann–Whitney U-test was used for ln, p, and q. Data are representative of at least two independent experiments (a, f, i, k, o), or pooled from three to six (be, g, h, ln, p, q) independent experiments. Source data are provided in a Source Data file