FAQ: What is the role of IL23/IL17 axis in IBD

Thank you to Johnson & Johnson for your support of this FAQ Video Module.

Inflammatory Bowel Disease (IBD) is a complex condition influenced by genetic, environmental, and microbial factors. In this FAQ video module, Amy Stewart, ARNP, from Capital Digestive Care in Washington, DC, explains the critical role of the IL-23/IL-17 axis in the pathogenesis of IBD. Supported by Johnson & Johnson, this discussion explores the cytokine-driven inflammatory pathways that contribute to chronic intestinal inflammation and how they can be targeted for effective treatment.

IL-23 (Interleukin-23) is a pro-inflammatory cytokine primarily produced by macrophages and dendritic cells in response to microbial stimulation. It plays a pivotal role in promoting chronic inflammation in IBD by inducing a unique inflammatory gene signature. This leads to the differentiation of T-helper 17 (Th17) cells, a specialized subset of T cells that drive inflammation. The activation of IL-23 receptors triggers a cascade of immune responses through the JAK-STAT signaling pathway, further amplifying the inflammatory process. Additionally, IL-17, a key cytokine regulated by IL-23, plays a major role in neutrophil activation and immune modulation, influencing both infection resistance and autoimmune pathology.

Given the central role of the IL-23/IL-17 axis in IBD and other autoimmune diseases, understanding these inflammatory pathways is crucial for developing targeted therapies. Many modern biologic treatments for IBD are designed to modulate these specific cytokines, helping to reduce inflammation and improve patient outcomes.

Join Amy Stewart, NP, in this expert discussion to gain deeper insights into the IL-23/IL-17 pathway and its implications for IBD treatment strategies. For more information and to explore the latest advancements in IBD care, visit the GHAPP website.