UPDATES
- Friday, 02 October
- 10:15 - 11:45 CEST
- Hall F2
Presentation details:
Diagnostic and therapeutic pearls in the skin of colour
Susan Taylor, United States
This presentation provides a practical, clinically focused overview of key diagnostic and therapeutic considerations in dermatologic diseases affecting patients with skin of color. Participants will gain insight into how common inflammatory and pigmentary disorders may present differently across diverse skin tones, with an emphasis on recognizing subtleties that can lead to delayed or missed diagnoses. The session will highlight characteristic morphological presentations of atopic dermatitis more frequently observed in skin of color, including follicular, papular, lichenified, and prurigo-like nodular. In addition, the lecture will address significant color variation in lesions associated with conditions such as psoriasis, seborrheic dermatitis, and acne, underscoring the importance of pattern recognition beyond erythema.
Therapeutic pearls will be shared to guide evidence-based and culturally competent management, including approaches to minimizing post-inflammatory hyperpigmentation, addressing keloidal scarring, and optimizing treatment outcomes in diverse patient populations. The session will conclude with practical strategies to improve diagnostic accuracy and therapeutic decision-making in everyday clinical practice.
Key Learning Objectives:
- Recognize distinct morphological patterns and color variations of common dermatologic conditions in skin of color to improve diagnostic accuracy
- Differentiate clinical presentations of inflammatory skin diseases in skin of color compared to lighter skin, with emphasis on atopic dermatitis, psoriasis, seborrheic dermatitis, and acne
- Apply tailored therapeutic strategies that address pigmentary sequelae, keloidal tendencies, and culturally competent care in patients with skin of color
New insights into the atopic inflammation
Kenji Kabashima, Japan
Atopic dermatitis (AD) is now understood as a disease driven by the interplay of three core elements — epidermal barrier dysfunction, type 2–skewed immune activation, and sensory nerve–driven itch. This “trinity” framework has recently been refined by advances in single-cell and spatial profiling, a deeper understanding of the neuroimmune circuits that sustain chronic itch and inflammation, and the maturation of targeted therapies. This lecture will first provide a concise overview of current AD pathophysiology, and will then focus on the most relevant developments of the past year — including new data on type 2 cytokines (IL-4/IL-13, IL-31, TSLP), the neuroimmune IL-31–IL-31RA axis, and JAK–STAT signaling — and how these insights translate into practical, day-to-day treatment decisions.
Key learning objectives:
- Summarize the current “trinity” model of AD pathogenesis, integrating skin barrier dysfunction, type 2 immunity, and neural sensitization of itch.
- Describe the most recent advances in the neuroimmune regulation of atopic inflammation, including the IL-31/IL-31RA axis and emerging cytokine targets.
- Apply these mechanistic insights to the selection and sequencing of modern targeted therapies — biologics and topical/oral JAK inhibitors — in clinical practice.
Mesenchymal stem cells in chronic wounds and tissue regeneration
Selim Aractingi, France
Chronic wounds, defined as wounds that fail to heal within 4–12 weeks, represent a major healthcare challenge worldwide. Most result from vascular, metabolic, or neurological disorders, and their burden include chronic pain, infection, malignant transformation, limb amputation and substantial healthcare costs. Despite decades of research, therapeutic innovation has remained limited. Advances have largely focused on improved wound dressings, while pharmacological approaches have been disappointing, with platelet-derived growth factor-BB remaining the only approved drug before its subsequent market withdrawal. Consequently, regenerative medicine, and particularly mesenchymal stromal cell (MSC) therapy, has emerged as one of the most promising strategies for promoting wound repair.
MSCs are primarily isolated from bone marrow, adipose tissue, umbilical cord, and placenta. Although the terminology remains heterogeneous in the literature—with terms such as mesenchymal stromal cells, adipose-derived stem/stromal cells (ASCs), and stromal vascular fraction (SVF) frequently used—consensus criteria have been established to define cultured MSCs. These cells express CD73, CD90, and CD105, while lacking CD34, CD45, and HLA-DR. Functionally, they are characterized by their capacity to differentiate into osteogenic, chondrogenic, and adipogenic lineages under appropriate culture conditions.
Because MSCs are present at low frequency in their native tissues, clinical applications generally require their isolation and ex vivo expansion before transplantation. Preclinical studies have consistently demonstrated that MSCs accelerate wound healing, primarily through paracrine mechanisms rather than direct tissue replacement. Their secretome promotes angiogenesis, modulates inflammation by favouring the transition from pro-inflammatory M1 to pro-reparative M2 macrophages, and stimulates endogenous tissue repair.
These encouraging findings have led to numerous clinical studies using predominantly autologous MSCs derived from bone marrow or adipose tissue, while a smaller number have investigated allogeneic cell products. Cells have been administered through several routes, including intralesional, perilesional, and intramuscular injection. In controlled studies comparing MSC therapy with standard care, sham procedures, or revascularization strategies, improved healing outcomes have frequently been reported. Several trials have described remarkably high healing rates and substantial reductions in major amputations.
Nevertheless, despite more than two decades of clinical investigation and consistently encouraging efficacy signals, no MSC-based therapy has yet achieved widespread regulatory approval for the treatment of chronic wounds. The biological, manufacturing, regulatory, and clinical factors that continue to limit successful translation into routine practice will be discussed. In addition, emerging regenerative strategies aimed at mobilizing endogenous fetal microchimeric cells in postpartum women will be presented as a potential alternative approach to enhance tissue repair.
Three learning objectives
- How mesenchymal stem cells (MSC) are defined and what are their main functions?
- Are MSC able to improve delayed wound healing in situations such as diabetes or arterial diseases?
- Why MSC are not yet readily available?