TRAF3 represses IL-17–induced expression of inflammatory factors in vivo. (A) TRAF3 expression was checked by immunoblotting (IB) with anti-TRAF3 from lysates of brain, spleen, and liver from two WT control mice (WT1 and WT2) or two TRAF3 transgenic founders (TG1 and TG2). (B and C) WT control or TRAF3 transgenic mice (T3TG; n = 4/group) were injected i.v. with adenovirus encoding empty vector (Ad-EV) or mIL-17 (Ad–IL-17) for 4 d. IL-17, KC, IL-6, and Mmp3 mRNA in the brain and spinal cord was measured by real-time PCR (B), and IL-17, IL-6, and KC protein in the serum was measured by ELISA (C). (D) TRAF3 expression was checked by immunoblotting with anti-TRAF3 from lysates of B16 cells and brain and spinal cord from four pairs of mice injected intracerebroventricularly with lentivirus encoding scrambled siRNA (siNC) or TRAF3 siRNA (siTRAF3). (E) C57BL/6 mice were injected intracerebroventricularly with lentivirus encoding scrambled siRNA or TRAF3 siRNA (n = 4/group) for 4 d and then were injected i.v. with adenovirus encoding empty vector or mIL-17 for 4 d. IL-17, KC, IL-6, and Mmp3 mRNA in the brain and spinal cord was measured by real-time PCR. mRNA expression is shown as fold of induction relative to that in the WT control mice. *, P < 0.05; and **, P < 0.01 (Student’s t test). Data are representative of three (A–C) or two (D and E) independent experiments (mean and SEM in B, C, and E).