Figure 6.

Cross-talk of NF-κB pathways in mouse aorta SMC stimulated with TNF and α-LTβR generates a phenotype resembling LTO. Cross-talk between TNFR-1–induced and LTβR-induced NF-κB target gene activation in SMC is likely to be attributable to p100 and RelB accumulation in response to TNF. Subsequent LTβR-mediated processing of the p100 inhibitor-to-p52 and nuclear translocation of p52-RelB complexes activates expression of molecules involved in adaptive immune responses, lymphorganogenic chemokines, and adhesion molecules in SMC.