ABSTRACT
Nuclear factor kappa В (NF-ĸB) regulates expression of a wide vari ety of cellular and viral genes (1-5). These genes include cytokines such as IL-2, IL-6, IL-8, GM-CSF, and TNF; cell adhesion molecules such as ICAM-1 and E-selectin; inducible nitric oxidase synthase (iNOS); and viruses such as human immunodeficiency virus (HIV) and cytome galovirus (6-16). Through the causal relationship with these genes, NFkB is considered to be causally involved in such currently intractable diseases as acquired immunodeficiency syndrome (AIDS), hematogenic cancer cell metastasis, and rheumatoid arthritis (RA). Although the genes induced by NF-kB are variable according to the context of cell lineage and are also under the control of other transcription factors, NFkB plays a major role in regulating the expression of these genes and thus contributes a great deal to the pathogenesis. It is notable that some of the target genes for NF-kB, such as IL-1 and TNF, are known to ini tiate the NF-kB activation cascade. Therefore, this cascade per se con stitutes a positive feedback loop unless inhibitors, such as IkB and IL IO, are produced. Therefore, biochemical intervention of NF-kB should
conceivably interfere with the pathogenic processes and would be ef fective for treatment.
