The global incidence of inflammatory bowel disease (IBD) has risen significantly in the past decade, making it a growing health concern.1 While biologic therapies have meaningfully improved disease management and patient outcomes including reduced surgical rates for disease complications, challenges have persisted with older molecules – with around one-third of patients failing to respond to induction therapy, and up to half of initial responders losing response over time.

Genome-wide association studies have identified variants in the IL23R gene, which encode the receptor for interleukin(IL)-23, and these variants have been linked to increased susceptibility for both Crohn’s disease (CD) and ulcerative colitis (UC).2 IL-23 plays a key role in the regulation of both innate immune and adaptive immunity, acting as a central regulatory cytokine. In addition, a growing body of evidence has supported the role of this cytokine in both the development and progression of IBD.3, 4, 5 As a result, IL-23 has gained prominence as a potentially critical therapeutic target.3, 5

In this narrative review, we explore the current understanding of IL-23 biology, and the downstream effector pathways that contribute to intestinal inflammation. We also discuss current and emerging strategies targeting IL-23 for the treatment of IBD.