Abstract
Psoriasis is a chronic inflammatory skin condition associated with immune dysregulation. The immunologic cascade mediated by the interleukin (IL)-17 pathway plays a critically important role in the pathogenesis of psoriasis. The IL-17 effectors (IL-17A, IL-17C, IL-17E, and IL17F) act on keratinocytes, endothelial cells, and immune cells to stimulate epidermal hyperplasia and the pro-inflammatory feed-forward cycle seen within plaque psoriasis. The IL-17 pathway is also hypothesized to modulate the inflammatory responses linking comorbid systemic diseases with psoriasis. Furthermore, the robust clinical response seen with current and emerging therapies targeting IL-17 emphasizes the importance of the IL-17 cytokines in the pathogenesis of psoriasis.
Compliance with Ethics Guidelines
This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.
Acknowledgments
This paper has not been previously published or posted and is not under consideration elsewhere.
Disclosure
Dr. Tina Bhutani has received research funding from Abbvie, Celgene, Galderma, Janssen, Pfizer, Regeneron, and Sun. She has served as an advisor for Abbvie, Boehringer-Ingelheim, Bristol Myers Squibb, Pfizer, Leo, Lilly, UCB, and Novartis. Dr. Wilson Liao has received research grant funding from Abbvie, Amgen, Janssen, Leo, Novartis, Pfizer, Regeneron, and TRex Bio. Megan Mosca, Julie Hong, Edward Hadeler, and Dr. Marwa Hakimi have nothing to disclose.