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.

Skin health in the modern world: Investigating the impact of environmental plastic pollutants on the skin barrier, skin immunity and allergic sensitisation

Grantee: Jessica Strid, Professor, Imperial College London, United Kingdom

Amount: DKK 3,999,159

Grant category: Research Grants

Year: 2026

Geography: United Kingdom

Genetics alone cannot account for the alarming increase in atopic dermatitis (AD) and allergic disease over the last few decades. Thus, we must look to understand the impact of environmental factors in the development of skin disease and allergy. Micro- and nanoplastics (MNPs), as well as chemical plasticizers, have become ubiquitous environmental contaminants. Albeit epidemiological data suggests a link between exposure to such plastic pollutants and development of AD and allergy, it remains unknown how they may impact on skin health and the immune system as a whole. This discovery study will define how MNPs and plasticizers affect skin immunity and characterise mechanism(s) whereby they regulate initiation of allergic disease. Results from this project will delineate how plastic pollutants may alter skin immunology and affect specific sensitisation pathways, thus elucidating new immune-therapeutic targets against skin barrier disruption, skin inflammation and allergy.

The impact of water hardness and water softeners on atopic dermatitis in Denmark: A national study

Grantee: Jakob Stokholm, Professor, Herlev and Gentofte Hospital/COPSAC, Denmark

Amount: DKK 3,943,851

Grant category: Research Grants

Year: 2026

Geography: Denmark

Atopic dermatitis (AD) is a frequent childhood skin disease with a substantial impact on patients’ daily lives. Its development is influenced by many factors, including genetics and the environment. Children in areas with hard water develop AD more often, but it is unclear why, whether other water compounds than the ones comprising hardness play a role, and also whether softening water can reduce risk. These will be the key elements to study in the current proposed project, which will evaluate how early-life drinking water composition affects the risk and severity of AD. This can be achieved by combining detailed water data with health information in two well-characterized mother-child cohorts and also in the entire Danish population. The findings may guide prevention strategies, inform caregivers, and provide evidence to support public health policies in Denmark regarding the health benefits of central water softening.

Elucidating the role of local inflammatory memory in skin

Grantee: Elodie Segura, Director of research, INSERM U1151, France

Amount: DKK 3,183,254

Grant category: Research Grants

Year: 2026

Geography: France

Immunological memory allows the immune system to respond more effectively to specific pathogens upon a second encounter. Another type of memory exists in some immune cells, ‘inflammatory memory’, allowing an enhanced response to a subsequent exposure to a pathogen that is different from the initial one. It remains unknown whether this type of memory also develops following injury-related inflammation, in the absence of a pathogen. In this project, we will explore this question in the skin, using a model of skin wound. We will focus in particular on the potential impact of this phenomenon on wound healing and on opportunistic infections with the bacteria Staphylococcus aureus. This research project will allow a better understanding of the impact of this ‘inflammatory memory’ on skin diseases, including relapsing-remitting disorders. In the longer term, results from this project should also create novel opportunities for the treatment of chronic wounds and immune-mediated skin damage.

From Skin Ulcer to Systemic Disease: Immunological Mechanisms and Therapeutic Targets in Pyoderma Gangrenosum

Grantee: Christian Vestergaard, Chair Professor, Aarhus University, Denmark

Amount: DKK 3,596,070

Grant category: Research Grants

Year: 2026

Geography: Denmark

Pyoderma gangrenosum is a rare but severe inflammatory skin disease that causes painful, non-healing wounds. In many patients, the skin disease is linked to inflammation in other organs, especially the gut, but it is not known how inflammation starting in the skin can spread through the body. This project uses a specially developed animal model that closely mimics the human disease, showing both skin ulcers and gut inflammation. Using state of the art biomolecular techniques we will study how immune cells and inflammatory signals move between skin and intestine, and we aim to understand how a local skin disease can become systemic. The results may help improve diagnosis and guide more targeted treatments for patients. The project is carried out within the framework of the DREAM Center, which brings together experts across medical disciplines to study complex inflammatory diseases affecting multiple organs.

Melanin-associated Extracellular Vesicle Communication in Skin Inflammation and Hyperpigmentation

Grantee: Cédric Delevoye, Director of Research, Institut Necker Enfants Malades (U1151), France

Amount: DKK 3,264,103

Grant category: Research Grants

Year: 2026

Geography: France

Skin color and protection from sunlight rely on the proper transfer of melanin from melanocytes to epidermal keratinocytes. In inflammatory skin conditions, this process is disrupted, causing abnormal pigment accumulation in dermal immune macrophage cells and leading to long-lasting dark spots known as post-inflammatory hyperpigmentation (PIH). The mechanism driving these alterations is poorly understood, which limits therapeutic options. Our work reveals that melanin particles are coated with biological messengers named extracellular vesicles (EVs). This project will investigate whether melanin-associated EVs actively control the fate of released pigments and pigmented cells under normal and inflammatory conditions. By combining molecular analyses with human skin models, MELCOM aims to clarify how inflammation disrupts pigment and immune-epithelial cell behavior. The result will provide new insights into inflammatory pigmentary disorders and identify potential therapeutic targets.

Prevention and Treatment of Atopic Dermatitis by RET Inhibition

Grantee: Carolyn Lee, Associate Professor, The University of Virginia, United States

Amount: DKK 3,999,301

Grant category: Research Grants

Year: 2026

Geography: USA

Atopic dermatitis (AD) is a chronic condition characterized by a weakened skin barrier, inflammation, and itch. Existing treatments mainly focus on relieving inflammation without directly addressing the skin barrier’s impairment. Our goal is to develop a topical treatment for AD that strengthens the skin barrier while reducing inflammation, an approach not previously explored. We recently discovered that a protein named RET is hyperactivated in AD, and inhibiting RET topically has shown promising results in enhancing the skin barrier and reducing inflammation. We hypothesize that topical RET inhibitors could effectively prevent and/or treat AD. Our proposal seeks to investigate how RET modulates skin barrier function and demonstrate the therapeutic effectiveness of topical RET inhibition using an established animal model that mimics human AD. This research is essential to fully explore RET as a therapeutic target in AD and advance the development of RET inhibitors for this condition.