Combined cytotoxic impairment and excess IL-18 leads to spontaneous CD8 T-cell activation and IFNg-dependent hyperinflammation. (A) tSNE plot of live splenic T cells from the indicated genotypes. (B) IFNγ production by CD8+ T cells following ex vivo stimulation. (C) Five-week-old Prf1−/−;Il18tg mice were treated with IFNg-neutralizing (clone XMG1.2) or control antibody for 2 weeks and then assessed for weight gain, spleen weight, Hb, platelet count, and serum CXCL9. *Adjusted P < .05, **P < .01, ***P < .001, ***P < .0001 by (B) 1-way ANOVA with Tukey post-test and (C) unpaired t test. Significance is only shown for comparisons where adjusted P < .05. Error bars represent SEM. Results are composites of 2 independent experiments with a minimum of 3 mice per genotype.
Figure 7.

Combined cytotoxic impairment and excess IL-18 leads to spontaneous CD8 T-cell activation and IFNg-dependent hyperinflammation. (A) tSNE plot of live splenic T cells from the indicated genotypes. (B) IFNγ production by CD8+ T cells following ex vivo stimulation. (C) Five-week-old Prf1−/−;Il18tg mice were treated with IFNg-neutralizing (clone XMG1.2) or control antibody for 2 weeks and then assessed for weight gain, spleen weight, Hb, platelet count, and serum CXCL9. *Adjusted P < .05, **P < .01, ***P < .001, ***P < .0001 by (B) 1-way ANOVA with Tukey post-test and (C) unpaired t test. Significance is only shown for comparisons where adjusted P < .05. Error bars represent SEM. Results are composites of 2 independent experiments with a minimum of 3 mice per genotype.

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