Fig. 5

MXC suppresses the autoimmunity caused by TREX1-deficiency. a Immunoblotting analysis of indicated proteins in L929 cells after transfected with nontargeting control siRNAs (siNC) or Trex1-specific siRNA (siTrex1) for 48 h and treated with 0.5 µg/ml HT-DNA for 3 h following a 6 h pretreatment with 500 µM MXC. b-d qPCR analysis of Ifit1 (b), Cxcl10 (c) and Isg15 (d) mRNA expression in Trex1-interfered L929 cells with the treatment of 500 µM MXC for 24 h. e Immunoblotting analysis of indicated protein from BMDMs of WT and Trex1^–/– mice. f, g Male (f) and female (g) Trex1^–/– mice were treated with MXC (30 mg/kg) daily for 14 days. Body weight was measured every day. h-l qPCR analysis of mRNA expression of indicated ISGs in WT and Trex1^–/– BMDMs treated with 500 µM MXC for 24 h. m-s WT mice (n = 3) were treated with PBS and Trex1^–/– mice (n = 6 per group) were given MXC (5 mg/kg, i.p.) for 7 days. Relative mRNA expression of indicated ISGs in mouse heart tissue was measured by qPCR. tTrex1^–/– mice (n = 10 per group) were given MXC (5 mg/kg, i.p.) or PBS for 90 days. The survival of mice was monitored. Statistical analysis was performed with a two-sided log-rank (Mantel-Cox) test. Data are presented as the mean ± s.e.m. *P < 0.05, **P < 0.01, ***P < 0.001. Data represent at least three biological independent experiments