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.
Decoding the Itch: a snapshot of how the IL-31 receptor switches on the signal to scratch in Atopic Dermatitis.
Grantee: Rosaria Gandini, Assistant Professor, Aarhus University, Denmark
Amount: DKK 3,700,678
Grant category: Research Grants
Year: 2026
Geography: Denmark
Atopic dermatitis (AD) is the most common chronic inflammatory skin condition worldwide. Its main symptom is chronic pruritus, an intense itch that severely disrupts patients’ sleep, mental health, and social well-being.
This urge to scratch is driven by a signalling molecule called Interleukin-31 (IL-31). To trigger the sensation of itch, IL-31 binds to a receptor on the cell surface transferring a signal to the inside that sets off a cascade of reactions. While this interaction is the key to unlocking the itch, the molecular details of the initiation mechanism remain a mystery.
Using Cryo-Electron Microscopy (cryo-EM), a Nobel Prize-winning imaging technique, we can “”take a snapshot”” of IL-31 binding to its full-length receptor. This knowledge can help to design better and more specific treatments, especially for patients who do not respond to the current ones, to shut down the itch where it starts.
TopiDLE: Preclinical Development of Topical Immunomodulatory Drugs (IMiDs) for the Treatment of Dicoid Lupus Erythematosus
Grantee: Cristina Solé, Dr., Vall d'Hebron Research Institute (VHIR), Spain
Amount: DKK 2,350,875
Grant category: Research Grants
Year: 2026
Geography: Spain
Discoid lupus erythematosus causes permanent scarring, hair loss and distress in over 500,000 people in Europe, predominantly women of childbearing age. When standard treatments fail, biological drugs exist but act systemically, cost around 10,000 euros per year, and are disproportionate for localised skin disease. Thalidomide as a pill achieves remission in 9 out of 10 patients, but causes nerve damage and is harmful in pregnancy, making indefinite treatment impossible.
We developed the world’s first topical thalidomide formulation: a cream that reduced lesions by 90% in mice while the drug stayed entirely in the skin, undetectable in blood, suggesting both risks could be eliminated.
This project will complete safety and efficacy studies to reach clinical trial, decode how the cream acts within the skin, opening the door to a new class of targeted topical drugs for autoimmune skin diseases, and identify biological markers to monitor treatment response without invasive procedures.
SkinmetaP – a platform to decode the functional landscape of human skin
Grantee: David Gomez Varela, Senior Scientist/Director of a Research Center, University of Vienna, Austria
Amount: DKK 3,244,717
Grant category: Research Grants
Year: 2026
Geography: Austria
Skin plays a major role in our well-being. Its role depends on a balanced molecular “conversation” between skin cells and the microorganisms living on its surface – the skin microbiome. When this balance is lost, diseases can develop.
Skin microbiome research has relied on DNA-based methods that reveal which microbes are present, but not what they are doing or how human cells respond. This limits progress toward precision dermatology, because the role of skin microbes in health depends less on who they are than on what they are doing – their function.
This project will develop a new technology, skinmetaP, to decode this functional conversation. We will measure thousands of human and microbial skin proteins from a simple, non-invasive swab.
SkinmetaP will allow us to create the first functional map of human skin in health and disease, revealing mechanisms that drive inflammation and treatment response – an important step toward better therapies and more personalized dermatological care.
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.
Stiffness matters: Engineering human skin model to treat skin fibrosis
Grantee: Yu Suk Choi, Associate Professor, The University of Western Australia, Australia
Amount: DKK 1,968,790
Grant category: Research Grants
Year: 2026
Geography: Australia
Our skin changes as we age, and one of the main reasons is that its layers gradually become stiffer, a process that is even more exaggerated in skin disease such as skin fibrosis. Surprisingly, these mechanical properties have received little attention in skin research. With new advances in mechanobiology, we now know that skin cells sense and respond to these mechanical changes. This project will create a realistic 3D human skin model using smart biomaterials that mimic the natural stiffness of each skin layer. By studying how skin cells behave in this lifelike environment over time, we aim to uncover how tissue mechanics contribute to skin health and disease. The insights gained may identify new treatment targets and support the development of “mechanotherapy”, therapies that work by gently adjusting the mechanical properties of skin to improve healing and reduce disease.
Development of a mast cell-integrated human skin equivalent as a standardized platform to study mast-cell biology and mast-cell-mediated inflammatory skin disorders
Grantee: Pål Johansen, Dep. Head of Research, University Hospital Zürich, Switzerland
Amount: DKK 2,541,401
Grant category: Research Grants
Year: 2026
Geography: Switzerland
Skin diseases such as mastocytosis, chronic hives, and atopic dermatitis involve immune cells called mast cells (MCs) and affect much people. Such conditions severely reduce quality of life, and many patients do not respond well to existing treatments. A major reason for the slow development of better therapies is that research still relies on animal models, which do not fully reflect human skin biology, or on limited patient samples. This project aims to address this problem by developing the first fully human, scaffold-free skin model that contains functional MCs. This innovative model closely mimics natural human skin and allows researchers to study how MCs cause inflammation and damage the skin barrier under realistic conditions. It will enable testing of new treatments directly in a human-based system, reducing the need for animal experiments. This project will improve our understanding of MC-driven skin diseases and help accelerate the discovery of better therapies for patients.
Early environmental and host factors for development of childhood atopic dermatitis: Unraveling the underlying proteomic and metabolomic pathways
Grantee: Nicklas Brustad, Associate Professor, Herlev and Gentofte Hospital/COPSAC, Denmark
Amount: DKK 3,998,278
Grant category: Research Grants
Year: 2026
Geography: Denmark
Atopic dermatitis is one of the most common childhood diseases with no effective prevention, which is urgently needed to reduce the number of children growing up with this disease. My ambition is to investigate whether the air pollution that children are exposed to, the environment they grow up in and the number of infections they contract in the first years of life are related to later development of childhood eczema. I will try to understand the mechanisms behind such relations and this is done by analyzing the pregnant mother and newborn child’s blood profiles, which may reveal which children are more prone to develop eczema based on how the environment shapes their blood profile. By looking for specific blood markers, we may be able to say exactly who is prone to develop eczema and our hope is to contribute the development of a strategy where simple blood tests can reveal how and which children that will develop eczema in the future.
VEGF-A as a therapeutic target in pemphigoid
Grantee: Kyle Amber, Associate Professor, Rush University Medical Center, United States
Amount: DKK 3,872,028
Grant category: Research Grants
Year: 2026
Geography: USA
Bullous pemphigoid (BP) is a serious blistering skin disease usually treated with long courses of steroids, which can cause major side effects. Despite advances in treatment, therapy for acute disease still relies heavily on prolonged high-dose oral corticosteroids. We found that a molecule called VEGF-A—known for driving inflammation—is much higher in the blood, and skin of people with BP. VEGF-A also rises alongside many other inflammatory signals. Early experiments in mice show that blocking VEGF-A can make the disease noticeably less severe. This project will test whether targeting VEGF-A can quickly reduce skin involvement in relevant models of pemphigoid. We will also study whether VEGF-A made specifically by skin cells is a key trigger of inflammation, and whether blocking VEGF-A in the skin (including with topical treatments) can help. The goal is to determine if VEGF-A could be a new, fast-acting, steroid-sparing treatment for BP.