- Deepak Balak, MD, PhD, MSc
- Congress Reports, Comorbidities, Genetics, Pathophysiology, & Epidemiology, Research, Treatment
The 54th Annual Meeting of the European Society for Dermatological Research (ESDR) was held in Antwerp, Belgium, from Wednesday, September 10 to Saturday, September 13, 2025. The event brought together more than 1,000 delegates from over 30 countries and languages, with basic, translational, and clinical science sessions. This report highlights the latest advancements in psoriasis research, including the IPC Symposium: Psoriasis, Differential Diagnosis, Paradoxical Responses, and New Treatment Mechanisms. Download the full 2025 ESDR Congress Report for complete details or read on for session summaries.
IPC SYMPOSIUM: PSORIASIS, DIFFERENTIAL DIAGNOSIS, PARADOXICAL RESPONSES, AND NEW TREATMENT MECHANISMS
Immune Shifts in Psoriasis
Michel Gilliet, MD, IPC Councilor
Professor Michel Gilliet outlined an immune module framework that classifies psoriasis into endotypes: Th17 for chronic plaque, type I interferon for acute and paradoxical presentations, and neutrophilic for pustular forms. Transcriptomic profiling showed that non-responders to Th17-targeted therapy often display a dominant type I interferon signature, indicating immune shifts during treatment. Aligning therapy with the prevailing module, for example, IL-23 or IL-17 blockade for Th17 disease, cyclosporin or TYK2 inhibition for interferon-dominant disease, improved outcomes and validated the module-guided approach.
Where Does Psoriasis Fit into the Differential Diagnosis of Contact Dermatitis?
Julien Lambert, MD, PhD
Professor Julien Lambert reviewed clinical and immunologic overlap between psoriasis and allergic contact dermatitis, particularly on the hands. Hyperkeratotic hand eczema can mimic palmoplantar psoriasis clinically and histologically, given shared Th17 and IL-36 activity. He emphasized indications for patch testing in therapy-recalcitrant, localized, pustular, or atypical disease, and when eosinophils are present on biopsy, to uncover contact allergy that may drive psoriasiform disease.
Paradoxical Psoriasis and Therapeutic Approaches
Paola Di Meglio, PhD, IPC Councilor
Professor Paola Di Meglio summarized paradoxical psoriasis across targeted therapies. TNF inhibitors are most frequently implicated, with a type I interferon surge as a key mechanism. Presentations range from plaque to palmoplantar pustular disease, with onset typically around 11 months. Management depends on severity and the primary condition, from topical or conventional systemic therapy to switching biologics, for example, IL-17 inhibitors when IBD is absent, or IL-12/23 or IL-23 inhibitors when IBD or mixed psoriasiform and eczematous features are present. JAK inhibitors are considered second-line.
Drug-Induced Psoriasis
Deepak Balak, MD, PhD, MSc, IPC Jr. Councilor
Dr. Deepak Balak reviewed drugs linked to de novo or exacerbated psoriasis, including beta-blockers, lithium, terbinafine, antimalarials, NSAIDs, and immune checkpoint inhibitors. Latency varies by agent, and morphology can shift, for example, from plaque to pustular. Because histology often mirrors idiopathic psoriasis, diagnosis relies on clinical context, latency, and medication review. A structured causality assessment and multidisciplinary management can clarify the role of medications and guide therapy changes.
Mechanisms of Topical Drug Delivery: Opportunities for Psoriasis?
Robert Rissmann, PhD
Professor Robert Rissmann highlighted advances in topical therapy, which is still central for mild disease and widely used in routine care. Impaired barrier function in psoriasis can increase penetration, while drug properties and vehicles determine delivery efficiency. Newer agents such as PDE4 inhibitors, aryl hydrocarbon receptor modulators, and improved vehicles and emerging microneedle systems offer enhanced efficacy and adherence. Future topicals target pathways including JAK signaling, senescence, immunometabolism, and the microbiome.
Oral Drug Development: History and Future Prospects
Curdin Conrad, MD, IPC Councilor
Professor Curdin Conrad traced the evolution from conventional orals, methotrexate, dimethylfumarate, acitretin, to modern small molecules such as PDE4 and TYK2 inhibitors. Next-generation oral strategies include cytokine-targeting peptides, for example, IL-23 receptor antagonists, and oral TNF inhibitors in development. He emphasized patient stratification by clinical phenotype and molecular endotype to match biologics or oral agents to the dominant immune pathway and phase of disease.
ABSTRACT PRESENTATIONS
Transcriptomic Profiling of Hyperkeratotic Hand Eczema Skin with Comparison to Atopic Dermatitis and Psoriasis
Weixin Zhou, MD
Dr. Weixin Zhou showed that hyperkeratotic hand eczema has a distinct lesional transcriptomic signature, with 2,000-plus differentially expressed genes, enriched for interferon-gamma signaling, T-helper pathways, and TRM cell markers, alongside downregulation of lipid metabolism and barrier genes. Compared with public psoriasis and atopic dermatitis datasets, hyperkeratotic hand eczema exhibited broader immune activation with pronounced TRM enrichment, supporting its classification as a separate immunopathologic entity.
Predicting Probability of Psoriasis Biologic Drug Continuation: An Explainable Machine Learning Approach Applying Real-World Data
Amaani Hussain
Dr. Amaani Hussain presented an explainable survival model trained on more than ten thousand biologic-naïve patients that predicted persistence up to 36 months with moderate performance. SHAP analyses identified initial biologic, age, recruitment center, occupational status, and baseline PASI as the most influential features. The model may support personalized selection by flagging individuals at higher risk of early discontinuation.
Chronic Hand Eczema is an IL-4Rα-Dependent Disease: Evidence from Integrated Clinical Trial and Molecular Profiling
Perrine Gery
Dr. Perrine Gery integrated phase 2b clinical and molecular data to show that chronic hand eczema is type 2 driven across subtypes. Dupilumab improved signs and symptoms and restored barrier and immune gene programs, reinforcing IL-4/IL-13 signaling as a central driver and supporting targeted therapy for moderate to severe disease.
Psoriatic Fibroblasts Exhibit a Distinct Transcriptomic Profile
Lili Flink Borbala
Dr. Lili Flink Borbala reported that fibroblasts from resolved psoriatic skin retain inflammatory and proliferative memory signatures compared with healthy controls, while never-lesional psoriatic skin shows subclinical alterations. Upregulated pathways included MAPK and IL-6 signaling, with transcriptional regulators such as TP53 and NOTCH4 differentially expressed, implicating dermal fibroblasts in recurrence and persistence beyond the epidermis.
Epithelial NF-κB Shapes the Innate and Adaptive Immune Landscape and Coordinates IL-17 Immunity
Divyaa Narayanan, BBiomed (Hons)
Ms. Divyaa Narayanan demonstrated that constitutive epithelial NF-κB activation in a murine model is sufficient to drive psoriasis-like disease, expanding macrophage and monocyte subsets and increasing IL-17-producing γδ T cells. Neutralizing IL-17a prevented and inhibited IL-17f, which ameliorated the phenotype, underscoring epithelial-immune crosstalk and the centrality of the IL-17 axis.
IL-34 Expression and Function in Hidradenitis Suppurativa and Psoriasis
Emanuele Scala, PhD
Dr. Emanuele Scala showed that IL-34, primarily produced by differentiated keratinocytes, is downregulated and mislocalized in lesional hidradenitis suppurativa and psoriasis. IL-34 supports tight junctions and barrier integrity, and its expression is restored after IL-17 or IL-23 blockade, suggesting a role as a biomarker of disease activity and treatment response
OTHER PSORIASIS SESSIONS
Editorial note: ESDR has now released official session videos. A single writer handled our onsite coverage, and several sessions ran concurrently. Our writer planned to prepare summaries from the recordings for sessions not attended in person. Since these videos were posted only recently, we will add the remaining summaries in the next few days.
Psoriasis and Epidermal Innervation
Laurent Misery, MD, PhD, and Matthieu Talagas
Summary coming soon.
From Rare to Frequent: How Immunogenetics Enlightens the Role of the Type I IFN Pathway in Psoriasis
Hervé Bachelez, MD, PhD, IPC Board Member
Summary coming soon.
Rethinking Psoriasis Management: Targeting Disease Memory for Long-Term Modification
Georg Stary, MD
Professor Georg Stary focused on tissue-resident memory T cells as drivers of relapse in previously involved skin. Early IL-23 inhibition reduced TRM populations more profoundly in superresponders and increased regulatory T cell balance, supporting a disease-modification approach that aims for durable remission beyond symptom control.
Early Intervention in Psoriasis: Guiding the Way to Disease Modification?
Enikö Sonkoly, MD, PhD
Professor Enikö Sonkoly presented data showing that patients with shorter disease duration are likelier to achieve complete clearance with IL-23 inhibition and enjoy longer drug-free intervals. Early, targeted therapy may prevent pathogenic TRM establishment, improving long-term control and delaying relapse.
Oral Peptides in Psoriasis: The Next Frontier in Treatment Innovation
Diamant Thaci, MD, PhD, IPC Councilor
Professor Diamant Thaci highlighted oral peptide therapeutics, including selective IL-23 receptor antagonists that achieved high IGA 0/1 and PASI 90 rates in phase 3 studies, with favorable tolerability and convenience. These agents combine biologic-like efficacy with oral delivery, positioning them as promising additions to systemic therapy.
Embracing the Known: Tracing the Evolution of Psoriasis
Lone Skov, MD, PhD, IPC Board Member
Professor Lone Skov traced the shift from a keratinocyte-centric view to a systemic, immune-mediated disease with distinct immune endotypes. She underscored heterogeneity across plaque, erythrodermic, and pustular disease, and the need to understand mechanisms behind biologic resistance to refine phenotype-driven, endotype-aware management.
Illuminating the Layers: Uncovering Immune Sophistication in Psoriasis
Curdin Conrad, MD, IPC Councilor
Professor Curdin Conrad described psoriasis as a dynamic immune continuum, early type I interferon activity transitioning to Th17 dominance. He advocated precision immunotyping and phase-specific interventions, including UV therapy for pDC depletion in guttate disease, PDE4 and TYK2 inhibitors for broad modulation, and cyclosporin for acute instability.
RNA-Based Modulation and Targeting of Skin Inflammation in Psoriasis and Atopic Dermatitis
Ana Rebane, PhD
Professor Ana Rebane presented RNA-based diagnostics, therapeutics, antisense oligonucleotides, siRNAs, and RNA mimics that modulate NF-κB, JAK-STAT, and IL-17 or IL-23 pathway activity. Preclinical data showed reduced inflammatory gene expression and improved barrier function, supporting future precision, possibly topical, RNA therapeutics.
Extracellular NAMPT Promotes Keratinocyte Hyperproliferation and Inflammation via TLR4 or TLR2 Pathways and Contributes to Psoriasis Symptoms in an Imiquimod-Induced Mouse Model
Luca Sanna, PhD
Dr. Luca Sanna identified extracellular NAMPT as a cytokine-like amplifier of psoriasis, upregulated by TNF-alpha and interferon-gamma. In keratinocytes, eNAMPT drove hyperproliferation and amplified IL-22-mediated inflammation via TLR2 signaling. Neutralizing eNAMPT reduced disease severity in an imiquimod model, positioning eNAMPT as a potential therapeutic target that bridges immune activation and epidermal dysfunction.
We encourage you to download the full 2025 ESDR Congress Report for detailed session summaries and in-depth coverage of findings.
