IL-23/IL-17 Axis Central to Psoriatic Arthritis Pathogenesis, Study Finds

A new review, published in Current Opinion in Rheumatology, outlines the critical role of the interleukin (IL)-23/IL-17 axis in the development of psoriatic arthritis, highlighting shared immune pathways that may inform evolving diagnostic and therapeutic approaches in dermatology and rheumatology.

Psoriatic arthritis (PsA), an immune-mediated disease characterized by inflammation in both the skin and joints, is increasingly understood to arise from converging autoinflammatory and autoimmune mechanisms. The review presents a concise yet comprehensive synthesis of current mechanistic insights, emphasizing the centrality of the IL-23/IL-17 axis in the disease's pathophysiology.

“This dual skin and joint clinical manifestation, which is characteristic of psoriatic arthritis and other rheumatic diseases,” the authors write, is driven by “mechanistic pathways” centered on innate and adaptive immune system activation. The IL-23/IL-17 axis, in particular, is identified as a unifying element across related rheumatic diseases, providing a framework for therapeutic targeting.

Recent advances in immunology have revealed that PsA and similar inflammatory arthritides share a core molecular architecture. The review highlights a shift in understanding the tissue origin of disease, suggesting that the bone marrow and other nontraditional sites may contribute to immune dysregulation.

“The interconnection between activated innate immune cells and adaptive immunity has transformed current thinking to include other organs such as the bone marrow as potential tissue of disease origin,” the study states.

These findings are supported by a range of preclinical models and genetic studies that converge on the IL-23/IL-17 signaling axis and implicate myeloid cell activation in the persistence of chronic inflammation. The review reinforces the concept that PsA, while clinically distinct from other rheumatic conditions, shares fundamental immunologic drivers that can be exploited for therapeutic benefit.

For clinicians, these insights support the rationale for biologic therapies targeting IL-17 or IL-23 pathways and encourage a broader understanding of PsA as a systemic inflammatory condition rather than an isolated joint or skin disease. The identification of shared pathogenic mechanisms also holds relevance for diagnosing overlapping syndromes and tailoring treatment strategies to patient-specific immune profiles.

The review also emphasizes the translational relevance of these findings: “These insights pave the way for the development of novel diagnostic and therapeutic strategies, with a focus on translating these findings into improved clinical practice.”

For dermatologists managing patients with psoriasis and musculoskeletal symptoms, this evolving mechanistic understanding reinforces the need for early recognition of PsA and collaboration with rheumatology colleagues. Targeted intervention at the level of the IL-23/IL-17 axis may not only control clinical symptoms but also interrupt disease progression and systemic inflammation.

Ultimately, the study affirms that continued integration of immunologic data into clinical frameworks is essential for advancing patient care in psoriatic disease. As therapeutic landscapes shift toward precision immunology, dermatologists must remain attuned to the shared molecular architecture that connects skin disease to systemic inflammation.

Reference
Saeed F, Adamopoulos IE. Pathogenesis of psoriatic arthritis: new insights from a bone marrow perspective. Curr Opin Rheumatol. 2025;37(2):136-141. doi:10.1097/BOR.0000000000001064