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. 2023 Oct 2;14:6132. doi: 10.1038/s41467-023-41892-5

Fig. 7. XQ2B suppresses systemic inflammation in Trex1−/− mice.

Fig. 7

a Trex1-/- BMDMs were treated with DMSO or XQ2B (10 μM) for 24 h, and induction of Ifnb1, Cxcl10 and Il6 mRNA was measured by qPCR. Fold changes are relative to WT BMDM group. p = 0.002 (Ifnb1); p = 0.008 (Cxcl10); p = 0.0005 (Il6). b Schematic representation illustrating the experimental design in the Trex1-/- mice model of autoimmune diseases. c Survival curves of WT and Trex1−/− mice treated with DMSO or XQ2B (10 mg/kg) every other day for 11 consecutive days (n = 10 mice per group). p = 0.0352. d WT mice (n = 6) or Trex1-/- mice (n = 6) were injected intravenously with DMSO or 10 mg/kg XQ2B every other day for 7 consecutive days. Representative H&E-stained tissue sections from WT or Trex1-/- mice treated with DMSO or XQ2B. The panels are at ×20 magnification. Scale bar, 100 μm. p = 0.0139 (Heart); p = 0.0139 (Stomach); p = 0.0274 (Tongue); p = 0.0315 (Kidney); p = 0.0139 (Muscle). e heart tissues from WT, Trex1–/– and Trex1–/– (XQ2B) mice (n = 5) were collected and induction of Ifnb1, Cxcl10 and Il6 mRNA was measured by qPCR. p = 0.0415 (Ifnb1); p = 0.0054 (Cxcl10); p = 0.0087 (Il6). f Antinuclear antibodies in WT, Trex1–/– and Trex1–/– (XQ2B) serum were detected using antinuclear antibody antigen substrate slide kit. Scale bar, 50 μm. Data are representative of two independent experiments with similar results in (f), or three independent experiments in (a) or two independent experiments in (d, e). (Data are presented as mean ± SD, n = 3 independent samples in (a); n = 6 mice per condition in (d); n = 5 mice per condition in (e), *p < 0.05, **p < 0.01, ***p < 0.001 using one-way ANOVA with Dunnett’s post hoc test). Source data are provided as a Source Data file.