A20 regulation of nuclear factor-κB: perspectives for inflammatory lung disease.
Persistent activation of NF-κB is central to the pathogenesis of many inflammatory lung disorders, including cystic fibrosis, asthma, and chronic obstructive pulmonary disease. A20 is an endogenous negative regulator of NF-κB signaling, which has been widely described in autoimmune and inflammatory disorders, including diabetes and Crohn's disease, but which has received little attention in terms of chronic lung disorders. This review examines the existing body of research on A20 regulation of NF-κB signaling and details the mechanism and regulation of A20 action focusing, where possible, on pulmonary inflammation. A20 and its associated signaling molecules are highlighted as being of potential therapeutic interest for the treatment of inflammatory disorders, and a proposed model of A20 activity in inflammatory lung disease is provided.
Queen’s University Belfast, Respiratory Research Cluster, Centre for Infection and Immunity, Belfast, United Kingdom.
Catriona
C
Kelly
Michael D
MD
Shields
J Stuart
JS
Elborn
Bettina C
BC
Schock
D000818:Animals; D054418:Chemokine CCL20 / Q000378:metabolism*; D002908:Chronic Disease; D042783:Endothelial Cells / Q000166:cytology; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation; D008168:Lung / Q000378:metabolism; D008171:Lung Diseases / Q000378:metabolism* / Q000382:microbiology; D051379:Mice; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism*; D017434:Protein Structure, Tertiary; D015398:Signal Transduction
D054418:Chemokine CCL20; D016328:NF-kappa B