JAK/STAT Pathway in Psoriasis and Psoriatic Arthritis: Insights into Inflammation and Tissue Remodeling

¹Des Moines University College of Osteopathic Medicine, West Des Moines, IA, USA

²Valley Consortium for Medical Education, Modesto, CA, USA

³Medical College of Georgia, Augusta University, Augusta, GA, USA

⁴University of New England College of Osteopathic Medicine, Biddeford, ME, USA

⁵A.T. Still University School of Osteopathic Medicine, Mesa, AZ, USA

⁶Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA

⁷Department of Dermatology, Northwell Health, New Hyde Park, NY, USA

*Corresponding author: Kelly Frasier, DO, MS, Department of Dermatology, Northwell Health, New Hyde Park, NY, USA, Phone: 3105956882, Email: [email protected]

Received Date: April 12, 2025

Publication Date: May 08, 2025

Citation: Misra R, et al. (2025). JAK/STAT Pathway in Psoriasis and Psoriatic Arthritis: Insights into Inflammation and Tissue Remodeling. Dermis. 5(3):38.

Copyright: Misra R, et al. © (2025).

ABSTRACT

The Janus Kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) pathway plays an important role in mediating inflammatory immune responses and is central to the development of psoriasis and psoriatic arthritis (PsA). Both of these conditions are caused by unregulated immune responses, with overlapping mechanisms specifically in its cytokine-mediated JAK/STAT activation. In psoriasis, the JAK/STAT signaling pathway has been linked to increased keratinocyte proliferation, the release of inflammatory cytokines, and the formation of characteristic skin plaques. In PsA, this same pathway has been demonstrated to drive joint damage, hyperproliferation of synovial cells, and pannus formation. Cytokines, such as interleukin (IL)-9 and IL-22, serve as common initiators of the JAK/STAT pathway in both psoriasis and PsA, leading to increased cellular proliferation in affected tissues. Recent studies show that blocking JAK signaling may not only lessen inflammation but also psoriasis-related keratinocyte proliferation and synovial tissue remodeling. These results highlight the dual modality of the JAK/STAT pathway in regulating pathogenic tissue alterations and inflammation in these linked disorders. By focusing on the common inflammatory pathways, JAK inhibitors have demonstrated promise in the clinical treatment of both psoriasis and PsA. However, the effectiveness of current medications on the market vary, therefore more research is necessary to look into particular JAK inhibitors that are best for both psoriasis and PsA. The purpose of this review is to organize the current understanding in both psoriasis and PsA pathophysiology as well as new developments regarding co-treatments of both psoriasis and PsA.

Keywords: Psoriasis, Arthritis, JAK/STAT, Orthopedic Surgery, Dermatology, Autoimmune, Degenerative Joint Disease