A20-Binding Inhibitor of NF-κB Activation 1 is a Physiologic Inhibitor of NF-κB: A Molecular Switch for Inflammation and Autoimmunity.

Abstract

The transcription factor NF-κB comprises a family of transcription factors critical for inflammatory signaling, and innate and adaptive immunity.1 NF-κB regulates the transcription of genes involved in immuno-inflammatory responses, cell survival, cell cycle progression, and cell adhesion. Activation of NF-κB by specific ligand-receptor interactions induces the expression of pro-inflammatory mediators, which orchestrate the recruitment of immune cells, induce the inflammatory response, and cause tissue injury.2,3 In this way, excessive NF-κB activity is considered harmful and a pathogenic factor in the chronic inflammation of numerous autoimmune disorders, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes, multiple sclerosis, and inflammatory bowel disease.4 Association between overactive NF-κB and autoimmunity emphasizes the importance of tightly controlled NF-κB signaling. One protein that regulates NF-κB signaling and maintains immune homeostasis is the A20 binding inhibitor of NF-κB1 (ABIN1).