Provide Immunologic Rationale For IL23 Directed Therapy in PsA, PsO, and IBD.

Join Heather Mambretti, PA-C, a rheumatology specialist in Houston, Texas, as she explores the critical role of IL-23 in autoimmune disease pathogenesis and how IL-23 inhibitors have revolutionized treatment strategies for psoriasis, psoriatic arthritis (PsA), and inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis.

IL-23 is a key cytokine produced by dendritic and macrophage cells, driving TH17 cell differentiation and fueling chronic inflammation. In psoriasis and PsA, dysregulated IL-23 signaling promotes TH17 proliferation, leading to increased IL-17A and IL-17F production—major contributors to inflammation in skin and joints. In IBD, IL-23 plays a similar role, disrupting intestinal barrier integrity and perpetuating chronic inflammation in conditions like Crohn’s disease and ulcerative colitis.

Targeting IL-23 with selective inhibitors has transformed the treatment landscape, offering a precise approach that reduces TH17-driven inflammation while preserving broader immune function. Clinical evidence, including a 2021 Rheumatology Journal publication, underscores IL-23’s pivotal role as the key link between skin, gut, and joint inflammation, making IL-23 inhibition an essential strategy in managing these autoimmune conditions.

IL-23 inhibitors provide effective, targeted therapy, reducing systemic inflammation, improving symptoms, and enhancing long-term patient outcomes across multiple inflammatory diseases.

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