TH1/cytotoxic: Lichen planus → Janus kinase (JAK) inhibitors
Matching therapy to the immune pattern predicted a response rate greater than 80%, whereas mismatched treatments failed, highlighting the clinical utility of immune profiling.
Rapid Molecular Readouts for Topicals
Robert Bissonnette, MD, chairman of Indero in 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.
Fibroblasts as Active Immune Regulators
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.
Mitochondria: Regulators of Skin Immunity
Rachael Clark, MD, PhD, of Brigham and Women’s Hospital in 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.
Translational Therapeutics
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 (NCT04882098) 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, connected chronic inflammatory dermatoses with CTCL, noting that 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-OX40L axis.