IĸBζ is a central modulator of inflammatory arthritis pathogenesis

Abstract

Current therapies targeting individual factors in inflammatory arthritis (IA) show variable efficacy, often requiring treatment using combinations of drugs and associated with undesirable side effects. NF-ĸB is critical for production and function of most inflammatory cytokines. However, given its essential role in physiologic processes, targeting NF-ĸB is precarious. Hence, identifying pathways downstream of NF-κB that selectively govern expression of inflammatory cytokines in IA would be advantageous. We have previously identified IĸBζ as a unique inflammatory signature of NF-ĸB that controls transcription of inflammatory cytokines only under pathologic conditions while sparing physiologic NF-ĸB signals.