rally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3]).
NF-κB activation can be detected in cultured synovial fibroblasts an