Asset Details
Do you wish to reserve the book?
The IL-23/IL-17 axis in Behçet’s syndrome pathogenesis: from immunological perspectives to therapeutic implications
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The IL-23/IL-17 axis in Behçet’s syndrome pathogenesis: from immunological perspectives to therapeutic implications
Do you wish to request the book?
The IL-23/IL-17 axis in Behçet’s syndrome pathogenesis: from immunological perspectives to therapeutic implications
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The IL-23/IL-17 axis in Behçet’s syndrome pathogenesis: from immunological perspectives to therapeutic implications
2026
Overview
Behçet’s Syndrome (BS) is a systemic vasculitis characterized by variable vessel involvement and an elusive etiology, though immunogenetic studies strongly implicate the IL-23/IL-17 axis which bridges innate and adaptive immunity, orchestrating type 17 T-cell responses thus modulating neutrophil function- with this cell a central player in both BS clinical features and immunopathology. Additionally, the contribution of Th1 cytokines—such as interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα)—reflects the broader immune plasticity observed in BS pathophysiology. Despite the immunogenetics incriminating the IL-23/IL-17 axis, clinical evidence confirming the role of IL-23/IL-17/inhibition in BS therapy is still limited including disappointing results with secukinumab in trials for Behçet’s uveitis. However, emerging evidence from small-scale retrospective studies, prospective trials, and case reports indicates that IL-23/IL-17 axis inhibition may benefit mucocutaneous and articular manifestations, as well as neuro-Behçet’s disease and the licensed PDE4 inhibitor apremilast regulates multiple aspects of IL-23/17 axis and neutrophil biology. Interestingly, anti-IL-17 therapy has been linked to BS induction. Herein, we discuss IL-23/IL-17 axis inhibition in BS and why it should be used cautiously and be limited to mucocutaneous and/or articular manifestations at this juncture. Further randomized controlled trials are imperative to dissect the IL-23/IL-17 axis in BS including high-dose anti-IL-23 therapy antagonism given that neutrophils are an abundant source of IL-23 and consider novel strategies including IL-23R antagonism.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Animals
/ Antigens
/ Behcet Syndrome - drug therapy
/ Behcet Syndrome - immunology
/ Behcet Syndrome - metabolism
/ Genes
/ Humans
/ Interleukin-17 - antagonists & inhibitors
/ Interleukin-23 - antagonists & inhibitors
/ Kinases
/ Review
/ Signal Transduction - drug effects
/ Skin
/ Ulcers
/ Uveitis
