In chronic inflammatory diseases, such as asthma, rheumatoidarthritis, inflammatory bowel disease, and psoriasis, severalcytokines recruit activated immune and inflammatory cells tothe site of lesions, thereby amplifying and perpetuating theinflammatory state.1 These activated cells produce many othermediators of inflammation.
What causes these diseases is still a mystery, but the diseaseprocess results from an interplay of genetic and environmentalfactors. Genes, such as those for atopy in asthma and for HLAantigens in rheumatoid arthritis and inflammatory bowel disease,may determine a patient's susceptibility to the disease andthe disease's severity, but environmental factors, often unknown,. . . [Full Text of this Article]
NF-B
The Role of NF-B in Inflammatory Diseases
Effects of Glucocorticoids on NF-B
Therapeutic Implications
Source Information
From the Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College, London (P.J.B.); and the Department of Pharmacology, University of California at San Diego, La Jolla (M.K.).
Address reprint requests to Dr. Barnes at the Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College, Dovehouse St., London SW3 6LY, United Kingdom.
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B — A Pivotal Transcription Factor in Chronic Inflammatory Diseases
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