The 2025 Inflammatory Skin Disease Summit unveils innovative therapies and immune profiling strategies, transforming the landscape of dermatological care.
The recent 2025 Inflammatory Skin Disease Summit in New York, New York, spotlighted cutting-edge research and emerging therapies, emphasizing mechanism-based care, immune profiling, and translational innovation. Speakers showcased how the field is moving beyond morphology to molecular and immune-guided strategies, reshaping diagnosis, treatment, and clinical trial design.
Brian Kim, MD, MTR, professor of dermatology and vice chair of research at the Kimberly and Eric J. Waldman Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York, reframed pruritus as a primary signal of systemic inflammation, not merely a superficial symptom. Itch often precedes visible lesions, making it a diagnostic biomarker. Mechanism-targeted therapies now go beyond symptomatic relief to address underlying inflammatory pathways.
Kim also highlighted bioelectronic medicine, including vagus-nerve stimulation, as a novel approach for patients refractory to biologics. By “tuning” immune responses rather than suppressing them, this strategy opens new avenues for chronic inflammatory and autoimmune skin diseases. He further emphasized molecularly informed trial designs, tailored to symptom-driven conditions such as chronic itch.
Kilian Eyerich, MD, PhD, chair and professor of dermatology at the University of Freiburg, Germany, advocated moving dermatology from morphology to immune mechanism–based classification. His 2-gene classifier (NOS2 and CCL27) distinguishes TH2, TH17, and TH1/cytotoxic inflammatory patterns, guiding therapy:
TH2:Atopic dermatitis → type-2 biologics
TH17: Psoriasis → IL-17–targeted therapies
TH1/cytotoxic: Lichen planus → JAK inhibitors
Matching therapy to immune pattern predicted greater than 80% response, while mismatched treatments failed, highlighting the clinical utility of immune profiling.
Robert Bissonnette, MD, chairman of Indero, Montreal, Canada, demonstrated that triamcinolone 0.5% cream produces clinical and molecular improvements in atopic dermatitis within 24 hours. Tape-strip transcriptomics revealed early normalization of Th2 pathways. This intrapatient, short-duration model may accelerate early-phase topical drug development, reducing costs and enabling faster translation to patient care.
Michael Rosenblum, MD, PhD, professor of dermatology at the University of California, San Francisco, revealed that PI16-expressing fibroblasts regulate inflammation, fibrosis, and pathogen containment. Disruption of neonatal Treg waves altered fibroblast and immune architecture, suggesting early-life determinants of disease susceptibility. Clinically, this identifies fibroblasts as therapeutic targets beyond conventional immune cells.
Rachael Clark, MD, PhD, of Brigham and Women’s Hospital, Boston, Massachusetts, presented mitochondria as master regulators of inflammation, independent of energy production. Interventions like tepinoroth modulate mitochondrial ROS and DAMP release, dampening inflammation in psoriasis and reversing immune evasion in mycosis fungoides. Low-dose radiation also triggers mitochondrial-mediated immune activation, offering novel approaches for immunomodulation and cancer therapy.
Massimo Gadina, PhD, editor in chief of the journal Inflammation and adjunct professor at Georgetown University in Washington, DC, highlighted the expanding role of JAK inhibitors in inflammatory skin and rheumatologic conditions. Long-term data from the APEX trial reinforced guselkumab’s ability to slow joint damage in psoriatic arthritis, underscoring the value of early intervention.
Patrick Brunner, MD, of the Icahn School of Medicine at Mount Sinai, New York, New York, connected chronic inflammatory dermatoses with CTCL, noting persistent tissue-resident T cells explain relapse after biologic withdrawal. Dupilumab-associated eruptions represent distinct immune states, emphasizing the need for nuanced interpretation.
Benjamin Ungar, MD, also of the Icahn School of Medicine at Mount Sinai, explored seborrheic dermatitis, barrier dysfunction, and inflammatory hair loss, highlighting emerging therapies targeting regulatory
T cells and the OX40-OX40 ligand axis.
Like what you’re reading? Subscribe to Dermatology Times for weekly updates on therapies, innovations, and real-world practice tips.
