73rd Annual Montagna Symposium on the Biology of Skin: Resident Memory T Cells in Health and Disease
Grantee: Professor, Dept of Dermatology, OHSU Alex Ortega Loayza, Oregon Health & Science University, USA
Amount: DKK 278,850
Grant category: Research Networking
Year: 2026
Geography: USA
The 73rd Annual Montagna Symposium, Resident Memory T Cells (TRM) in Health and Disease, will be held October 15-19, 2026, in Oregon’s scenic Columbia River Gorge. TRM are specialized cells that protect against known pathogens, but when inappropriately activated, they can cause diseases such as psoriasis, vitiligo, and rheumatoid arthritis.
The Symposium will share insights into TRM generation, persistence, and contribution to disease; examine how drugs affect TRM; and investigate avenues for leveraging TRM toward cures for chronic inflammatory and autoimmune diseases.
This event is designed for senior- and junior-level scientists; clinicians; clinical, translational, and basic science researchers; industry representatives; patient advocates; and trainees. The format includes lectures, discussion, and networking opportunities that foster interaction between new and established scientists and dermatologists. Visit https://montagnasymposium.org/ for the program and registration.
The 2027 Gordon Research Conference on Epithelial Differentiation and Keratinization
Grantee: Associate Professor Ryan Driskell, Washington State University, USA
Amount: DKK 357,053
Grant category: Research Networking
Year: 2026
Geography: USA
The 2027 Gordon Research Conference on Epithelial Differentiation and Keratinization will take place June 6-11, 2027 at the Rey Don Jaime Grand Hotel in Castelldefels, Barcelona, Spain, with a trainee-led Gordon Research Seminar on June 5-6. The meeting will bring together international scientists studying how skin forms, maintains its barrier, repairs wounds, and fails in diseases such as inflammatory skin disorders, inherited barrier defects, alopecia, and cancer. The program will combine developmental biology, stem-cell biology, regeneration, human disease, and computational/spatial technologies. LEO Foundation support will help international speakers and young researchers attend, present unpublished work, receive mentoring, and build collaborations that advance skin research.
A Non-Invasive Genomic and Transcriptomic Decision-Assist Tool for Suspected Subungual Melanoma
Grantee: Beth McLellan, Professor and Chief, Albert Einstein College of Medicine
Amount: DKK 3,999,656
Grant category: Serendipity Grants
Year: 2026
Geography: USA
While studying skin bacteria, we made a surprising discovery: simple, painless nail clippings contain readable human genetic messages (mRNA). Scientists previously believed these delicate messages were completely destroyed as nail cells harden and die. This unexpected finding could revolutionize how we diagnose subungual melanoma, a deadly skin cancer growing under the nail. Currently, diagnosing this cancer requires a painful surgical biopsy of the nail bed, risking permanent deformity. Our discovery suggests we might detect this cancer, and understand its deeper biology, just by analyzing a painless clipping. To investigate this, we will collect nail clippings from patients with harmless dark spots and those with confirmed nail cancer. Using advanced technology, we will read the surviving genetic messages to identify a “signature” of the cancer. We will also explore if these clippings reveal how the tumor interacts with the immune system, paving the way for pain-free diagnostics.
Nasal microbiota as a novel axis for skin immune regulation
Grantee: Erin (Yiyin) Chen, Assistant Professor (MIT), Core Institute Member (Broad Institute)
Amount: DKK 3,999,997
Grant category: Serendipity Grants
Year: 2026
Geography: USA
We aim to understand how skin inflammation is suppressed by a surprising site: the nose. This proposal is motivated by two unexpected discoveries during our prior Leo-funded work. First, we found that some bacteria generate large immune responses when they colonize the nose peacefully, even when there is no evidence of infection. Second, we found that these nasal bacteria suppress the immune response in the skin, even though the skin is 100x larger than the nose. Therefore, we hypothesize that the nose is an overlooked site of immune regulation for the skin. We now aim to understand the molecular details of this nose-skin immune suppression. We also plan to study how nose-skin immune suppression changes our risk of eczema, psoriasis, infection, and cancer. Overall, we hope to understand how the bacteria that naturally colonize our nose regulate skin health and use these insights to develop new therapies for skin inflammation.
Integrating Optical Imaging and Single-Cell Spatial Omics to Uncover Biomarkers of Vitiligo Repigmentation
Grantee: Kavita Sarin, Professor, Board of Trustees of the Leland Stanford Junior University, United States
Amount: DKK 4,775,516
Grant category: Research Grants
Year: 2026
Geography: USA
Vitiligo is a skin condition caused by the progressive loss of pigment cells, leading to white patches on the skin. The condition becomes active and detectable at a cellular level long before visible skin changes are observed. However, current methods to detect such cellular-level damage require invasive biopsies. Our project will enable preventative treatments and monitoring using a noninvasive imaging tool. By combining optical imaging with spatial omics, we will develop the first cellular-level map of vitiligo without the need for biopsies. This innovative tool will use artificial intelligence to identify specific cell types and monitor disease progression in real time. This approach promises to enhance early detection and treatment of vitiligo and has potential applications for various other skin conditions, such as inflammation and cancer. Ultimately, this could lead to more personalized and effective treatments, improving patient outcomes and accelerating drug development.
WARS1–TLR4 signaling links interferon priming to UV-induced myeloid activation in photosensitive skin
Grantee: Manuel Garber, Professor, University of Massachusetts Medical School, United States
Amount: DKK 3,951,363
Grant category: Research Grants
Year: 2026
Geography: USA
Cutaneous lupus erythematosus (CLE) is a skin disease in which sunlight, instead of calming the immune system, triggers painful and damaging inflammation. This unusual reaction is poorly understood, making it difficult to prevent disease flares.
Our research has identified a group of immune cells in the skin that become highly inflammatory after sun exposure and drive tissue damage. However, the signal that activates these cells remains unknown.
We propose that a stress-related protein released by skin cells after UV exposure acts as a trigger that turns these immune cells into harmful inflammatory cells. To test this, we will study human skin samples and examine how blocking or adding this signal affects immune activation.
Understanding this mechanism could lead to new strategies to prevent sun-induced flares in lupus and related diseases.
Leveraging Demodex mites to decode inflammatory mechanisms in skin diseases
Grantee: Roberto Ricardo-Gonzalez, Associate Professor, The Regents of The University of California San Francisco, United States
Amount: DKK 3,999,258
Grant category: Research Grants
Year: 2026
Geography: USA
Demodex mites usually live harmlessly and at low levels in facial hair follicles and sebaceous glands. Still, in some people, they become overabundant and are linked to chronic inflammatory skin diseases such as rosacea. The key problem is understanding why the immune system sometimes tolerates these mites and other times triggers persistent inflammation. Our research aims to identify the molecular “switch” that determines this outcome. Using a mouse model of Demodex infection and novel Demodex-keratinocyte co-culture systems, we discovered that a signaling pathway involving IL-36 and gasdermin proteins activates protective type 2 immune cells that control mites. However, when dysregulated, this same pathway may drive excessive inflammation. By defining how skin cells sense Demodex and regulate immune responses, we aim to uncover new, targeted treatments for rosacea and other inflammatory skin conditions linked to microbial imbalance.
Ancestry-Linked IL1A Variant at 2q13 as a Driver of Keratinocyte IL‑1 Signaling and Skin Inflammation
Grantee: Lam Tsoi, Associate Professor, University of Michigan, United States
Amount: DKK 4,046,399
Grant category: Research Grants
Year: 2026
Geography: USA
Inflammatory skin diseases can be more common and severe in people of African ancestry, but the biological reasons are unknown. Our work shows that healthy skin from individuals of African ancestry has elevated interleukin 1 (IL 1) signaling, and that a specific DNA region regulating this pathway carries a variant with higher frequency among individuals of African ancestry. This project will provide mechanistic understanding of how this genetic difference changes the way skin cells sense and respond to IL 1 signaling. We will edit the variant in human skin cells and read out the effects at single cell resolution, both in the lab and in donated skin samples. By revealing how inherited differences in skin regulation drive susceptibility to inflammation, the project will lay the groundwork for ancestry aware, more precise treatments that better control disease and help reduce inequities in skin health.
Rational Design of Dual PDE4/JAK Inhibitors with Reduced Blood-Brain Barrier Penetration for Treatment of Inflammatory Skin Diseases
Grantee: Christopher Bunick, Associate Professor of Dermatology, Yale University, United States
Amount: DKK 3,751,536
Grant category: Research Grants
Year: 2026
Geography: USA
Many skin conditions like eczema, psoriasis, and hair loss are caused by an overactive immune system. Two types of medications, PDE4 inhibitors and JAK inhibitors, can calm this immune response, but each has drawbacks. PDE4 inhibitors can cause nausea and headaches because they enter the brain, while JAK inhibitors may increase infection risk. Our research asks: what if we combine both medications at lower doses? This could provide better, synergistic treatment with fewer side effects. Building on our previous work understanding how these drugs work at the molecular level, we will use artificial intelligence and computer simulations to: (1) predict which drug modifications prevent brain entry; (2) find the best drug combinations; and (3) design new, safer medications. We expect this research could lead to more effective treatments for many people with inflammatory skin diseases, with fewer side effects than current options, improving the patient standard of care.
Modeling and targeting bullous pemphigoid in skin organoids
Grantee: Karl Koehler, Associate Professor of Otolaryngology-Head and Neck Surgery, The Childrens Hospital Corporation (d/b/a Boston Children's Hospital), United States
Amount: DKK 3,998,920
Grant category: Research Grants
Year: 2026
Geography: USA
Bullous pemphigoid (BP) is a skin disease in which the immune system attacks a protein called BP180 that helps hold the layers of the skin together. This causes itching, inflammation, and blistering, mainly in older adults. BP is becoming more common as the population ages, and it is still associated with a relatively high risk of death, showing the need for better treatments.
Research has been limited because current BP models are not close to real human skin. In this project, we will use human stem cells to grow miniature skin tissues, called skin organoids, that mimic key features of human skin. We will expose these organoids to disease-causing BP antibodies to study how skin damage begins, how the skin becomes fragile, and how the immune reaction develops. This work will improve our understanding of BP, reveal possible treatment targets, and create a new human model for developing and testing future therapies.