Describe the IL-23/IL-17 Axis

Welcome to this FAQ video module, proudly supported by Johnson & Johnson. In this educational session, Erica Heagy, NP, from Alaska Digestive and Liver Disease, explores the IL-23/IL-17 axis, a crucial pathway in the pathogenesis of inflammatory bowel disease (IBD), psoriasis, psoriatic arthritis, multiple sclerosis, and other immune-mediated disorders.

The IL-23 cytokine plays a pivotal role in promoting Th17 cell differentiation, which in turn produces pro-inflammatory cytokines like IL-17A, IL-17F, tumor necrosis factor (TNF), and IL-6. IL-17, a key driver of chronic inflammation, is overexpressed in patients with autoimmune diseases, contributing to tissue damage, immune dysregulation, and inflammation. These effects are particularly evident in conditions such as Crohn’s disease, ulcerative colitis, and psoriatic arthritis, making the IL-23/IL-17 axis a major target for emerging biologic therapies.

Therapeutic strategies that block IL-23 or its receptor have been FDA-approved for treating psoriasis, psoriatic arthritis, and IBD. By inhibiting this inflammatory pathway, these treatments help reduce disease progression, alleviate symptoms, and improve patient outcomes. Understanding this mechanism is essential for healthcare providers seeking optimized, targeted treatment options for their patients.

For more information on IL-23-targeted therapies and advances in gastroenterology, hepatology, and immune-mediated disease treatment, visit GHAPP.org or download the GHAPP ACE mobile app on Android or IOS. Stay connected with us on LinkedIn, YouTube, X (formerly Twitter), and Instagram for expert insights and updates.