Figure 1: Stk38 deficiency increases TLR9-mediated inflammatory responses.

(a) ELISA assay of IL-6 in the supernatants of RAW264.7 cells stably transfected with Stk38 shRNA and control (Ctrl) vector, stimulated with 100 ng ml⁻¹ LPS, 5 μg ml⁻¹ LTA or 10 μg ml⁻¹ CpG for 6 h. Data are shown as mean±s.d. (n=3). **P<0.01 (Student’s t-test). Similar results were obtained in three independent experiments. (b) Cells as in a were stimulated with 100 ng ml⁻¹ LPS or 10 μg ml⁻¹ CpG for 1.5 h. TNF-α and IL-6 mRNA expression in the cells was detected by real-time PCR. Data are shown as mean±s.d. (n=3). **P<0.01 (Student’s t-test). Similar results were obtained in three independent experiments. (c) ELISA assay of TNF-α and IL-6 in the supernatants of wild-type (WT) and Stk38-deficient (Stk38^−/−) mouse peritoneal macrophages stimulated with 100 ng ml⁻¹ LPS, 5 μg ml⁻¹ LTA or 10 μg ml⁻¹ CpG for 6 h. Data are shown as mean±s.d. (n=3). **P<0.01 (Student’s t-test). Similar results were obtained in three independent experiments. (d) Wild-type (WT) and Stk38-deficient (Stk38^−/−) mouse peritoneal macrophages were stimulated with 100 ng ml⁻¹ LPS or 10 μg ml⁻¹ CpG for 1.5 h. TNF-α and IL-6 mRNA expressions were detected by real-time PCR. Data are shown as mean±s.d. (n=3). **P<0.01 (Student’s t-test). Similar results were obtained in three independent experiments.