Figure 4. TLR2 stimulation prevents binding of general transcriptional machinery to the CIITA and CXCL11 promoters.

BMDM were treated with 10 ng/ml Pam₃CSK₄ for 8–9 h, then 20 ng/ml IFN-γ for 4 h. Cross-linked DNA was sheared and immunoprecipitated with anti-PolII (A) or anti-TBP (B) antibodies. Precipitated and input DNA for each sample were assayed by qPCR with primers specific for the transcriptional start site in the promoters of CXCL11, CIITA, and NOS2 (A) or the TATA box of the CXCL11 promoter (B). All values were normalized to GAPDH. Results are expressed as fold increase over untreated controls and are the mean of triplicate samples±SD. Statistical significance between IFN-γ alone samples and Pam₃CSK₄ prior to IFN-γ treated samples was determined by two-tailed t-test. Results are representative of at least two independent experiments.