Session Information
Date: Sunday, October 26, 2025
Title: (0098–0114) Spondyloarthritis Including Psoriatic Arthritis – Basic Science Poster
Session Type: Poster Session A
Session Time: 10:30AM-12:30PM
Background/Purpose: Psoriatic arthritis (PsA) is a chronic inflammatory disease for which TNFα inhibitors are the standard first-line biologic therapy. Nonetheless, a significant proportion of patients exhibit an inadequate response, requiring a switch to alternative agents. There are several second-line treatment options, such as IL-17 inhibitors, IL-23 inhibitors, or JAK inhibitors. Among these options, IL-23 inhibitors are increasingly used, yet there is no clear guidance to inform their selection in clinical practice. Exploring how TNFα inhibition influences the IL-23 levels may offer valuable insights into whether anti-IL-23 therapies represent a rational and effective choice after anti-TNF failure. This study aims to investigate the effect of anti-TNFa therapy on IL-23 serum levels in PsA patients and explore the mechanistic regulation of IL-23 and other inflammatory markers by TNFa in vitro.
Methods: Serum IL-23 levels were measured by ELISA in a cohort of 40 PsA patients before and after six months of anti-TNFa therapy. In parallel, primary human dermal fibroblasts were cultured and stimulated with recombinant TNFα in the presence or absence of anti-TNFα agents using varying concentrations and exposure times (6h, 24h and 48h). IL-23 expression and other key inflammatory markers were assessed by RT-qPCR to evaluate the impact of TNFα blockade.
Results: Serum IL-23 levels were significantly reduced after six months of anti-TNFα therapy. In vitro, TNFα stimulation induced a robust upregulation of IL-23 expression in dermal fibroblasts which was effectively reversed by anti-TNFα agents. Additionally, anti-TNFα exposure led to a significant decrease in the expression of inflammatory mediators such as IL-6, while genes like IL-17 remained largely unchanged. These findings suggest that TNFα directly promotes IL-23 production in resident skin cells, and that its inhibition downregulates this axis both systemically and at the tissue level.
Conclusion: Our findings demonstrate that anti-TNFα therapy significantly modulates key inflammatory pathways in PsA. Anti-TNFα treatment leads to a notable reduction in IL-23 levels both in vivo and in vitro, highlighting IL-23 as a downstream target of TNF signaling in PsA. Therefore, quantification of IL-23 could serve as a promising biomarker for personalizing biologic sequencing and guiding second-line therapy selection in PsA patients with suboptimal responses to anti-TNFα agents. Acknowledgements. Project ” PMP21/00119″, funded by Instituto de Salud Carlos III (ISCIII) and co-funded by the European Union.
To cite this abstract in AMA style:
Martín Salazar J, López Medina C, Pérez Sánchez C, Puche-Larrubia M, Ortiz Buitrago P, López-Montilla M, Arias de la Rosa I, Cuesta López L, Ruiz Ponce M, Barranco A, Romero Zurita L, Moreno-Caño E, Ortega-Castro R, Calvo J, Abalos-Aguilera M, Ruiz-Vilchez D, López pedrera C, Escudero Contreras A, Collantes estévez E, Barbarroja N. In Vivo and In Vitro Analysis of IL-23 Modulation Following Anti-TNF Therapy in Psoriatic Arthritis [abstract]. Arthritis Rheumatol. 2025; 77 (suppl 9). https://acrabstracts.org/abstract/in-vivo-and-in-vitro-analysis-of-il-23-modulation-following-anti-tnf-therapy-in-psoriatic-arthritis/. Accessed .« Back to ACR Convergence 2025
ACR Meeting Abstracts - https://acrabstracts.org/abstract/in-vivo-and-in-vitro-analysis-of-il-23-modulation-following-anti-tnf-therapy-in-psoriatic-arthritis/