CHAPEAU GLOBAL
Grantee: Hanna Bonnekoh, Dermatologist, Allergist, Charité - Universitätsmedizin Berlin, Institute of Allergology, Germany
Amount: DKK 3,118,599
Grant category: Research Grants
Year: 2026
Geography: Germany
Acute urticaria (hives) is a common skin disease affecting up to 1 in 5 people during their lifetime. In many patients the condition disappears within weeks, but in some it develops into chronic spontaneous urticaria, which can persist for years and significantly reduce quality of life. At present, it is unclear why some patients recover while others develop a chronic disease. The CHAPEAU GLOBAL study aims to better understand the biological processes behind this transition. Researchers will analyze blood samples from patients with acute urticaria at two time points and compare those who recover with those who later develop chronic urticaria. Using advanced laboratory methods, thousands of proteins and immune markers will be examined to identify early warning signs of chronic disease. The goal of this international study is to identify patients at risk earlier and improve prevention and treatment strategies for chronic urticaria.
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.
From Barrier to Bioreactor: Harnessing Local Antigen Presentation in Skin
Grantee: Janin Chandra, Senior Research Fellow, Group Leader, The University of Queensland, Australia
Amount: DKK 4,000,000
Grant category: Research Grants
Year: 2026
Geography: Australia
The skin constantly decides when to defend the body and when to avoid unnecessary inflammation. CD4 T cells help make these decisions, but they rely on other cells to show them “danger signals” through a molecule called MHC-II. Until recently, only specialised immune cells were thought to use this pathway. New evidence, including our own, shows that ordinary skin cells such as keratinocytes and fibroblasts can also switch on MHC-II and directly influence T cell behaviour, representing a major shift in how skin immunity is understood. This project will uncover when these non-immune cells use MHC-II, whether they can guide T cell responses, and how this affects vaccines delivered into the skin. Understanding this newly recognised pathway will help explain why some skin conditions become chronic, why others resolve, and how we can design better treatments and vaccines that work with the skin’s built-in immune machinery.
Nutritional Metabolic determinants of skin tissue in Buruli ulcer progression and recovery
Grantee: Aloysius Loglo, Postdoctoral Research Fellow, Kumasi Centre for Collaborative Research in Tropical Medicine (KCCR), Ghana
Amount: DKK 3,997,701
Grant category: Research Grants
Year: 2026
Geography: Ghana
Buruli ulcer is a severe skin disease common in rural West Africa, caused by flesh-destroying bacteria. While antibiotics kill the bacteria, many patients suffer from extremely slow wound healing, leading to long hospital stays and disability. We have found that patients with this disease often lack essential nutrients like zinc and vitamin C, which are crucial for the body to heal and fight off infections.
This project will investigate how the human body processes nutrients (metabolism) and how gut health affects a patient’s ability to heal. We will study the wound itself, blood and stool of 80 participants to look for specific chemical markers linked to fast or slow healing. We will also investigate how changing weather patterns and poor sanitation affect food availability and gut health, putting people at higher risk. Ultimately, we aim to develop targeted nutritional treatments that can be given alongside antibiotics to help thousands of patients heal faster across West Africa.
Uncovering the Role of Crinophagy in Melanosome Homeostasis and Pigmentation Disorders.
Grantee: Marta Giacomello, Associate Professor, University of Padua, Department of Biology, Italy
Amount: DKK 4,995,299
Grant category: Research Grants
Year: 2026
Geography: Italy
Crinophagy is a natural process occurring in secretory cells, where cellular “packages” called secretory granules are broken down by lysosomes, the cell’s recycling centers, without using the standard degradation pathway called autophagy. Crinophagy preserves cell homeostasis and is characterized by distinctive intracellular structures named crinosomes. These are cluster of secretory granules targeted for degradation. While studying mitochondria–melanosome interactions via Mitofusin2, we observed large melanosome clusters enclosed by a single membrane, resembling crinosomes. Combined with evidence that some crinophagy proteins influence pigmentation, this suggests crinophagy may occur in melanocytes. In this project we aim to verify if crinophagy contributes to melanosome turnover and skin pigmentation, and to enhance our understanding of the etiology of rare pigmentation disorders, like Chediak–Higashi and Hermansky–Pudlak syndromes, which feature abnormal, enlarged melanosomes.
Building on discovery to develop a phage therapeutic for Group A Streptococcus necrotising soft tissue infection
Grantee: Thomas Sicheritz-Pontén, Professor, University of Copenhagen, Denmark
Amount: DKK 3,999,634
Grant category: Research Grants
Year: 2026
Geography: Denmark
Necrotising Soft Tissue Infections, (flesh eating disease), are rapidly progressing, life threatening infections mostly caused by Group A Streptococcus. Current treatments are surgery and antibiotics, but are often insufficient leading to high rates of amputation and death.
This project develops phage therapy as a targeted alternative. Building on our previous work where we identified the first effective phages against GAS, we will expand and test phages and use computational models to design optimal phage cocktails that maximise bacterial coverage while reducing resistance risk.
To enable effective treatment in infected tissue, we will develop a hydrogel based delivery system to stabilise and deliver phages locally. The most promising therapies will be tested in advanced human skin models that mimic NSTI.
The aim is to create a new, targeted therapeutic approach, that complements existing treatment, improves infection control, and reduces the need for surgery and amputation.
Precision Vitiligo Immunotherapy via Nanocarrier-Enabled Microneedles
Grantee: Georgios Sotiriou, Professor, Stockholm University, Sweden
Amount: DKK 4,000,000
Grant category: Research Grants
Year: 2026
Geography: Sweden
Vitiligo is a condition where the immune system mistakenly attacks pigment-producing skin cells, causing white patches. While powerful new drugs called biologics can stop this, taking them via whole-body injections causes severe side effects. Since vitiligo is localized to the skin, treating the whole body is risky. However, these fragile drugs cannot easily cross the skin’s tough barrier on their own.
We are solving this by developing a painless “”smart patch”” covered in dissolving microneedles. To protect the delicate biologic drugs, we first pack them into tiny nanocarriers made from a natural mineral. These protected drugs are then embedded into the microneedles. When applied to the affected skin, the needles painlessly penetrate and dissolve, releasing the medicine exactly where the immune cells are misbehaving.
This project aims to provide a safe, highly effective way to halt vitiligo locally, without shutting down the patient’s entire immune system.
Targeted stabilization of ATP2A2 mRNA using small RNA therapeutics as a treatment strategy for Darier’s disease
Grantee: Søren Lykke-Andersen, Academic employee, Aarhus University, Denmark
Amount: DKK 3,999,978
Grant category: Research Grants
Year: 2026
Geography: Denmark
Darier’s disease is a rare skin disorder causing painful skin lesions, recurrent infections, and profound psychosocial burden, including depression. No treatment addresses the underlying cause – patients manage symptoms with limited, poorly tolerated therapies.
The disease results from a fault in one copy of the ATP2A2 gene, leaving skin cells with insufficient levels of SERCA2, a protein critical for calcium signaling. The other copy remains intact.
Our approach exploits this: rather than replacing the faulty gene, we use a small engineered RNA molecule to stabilize the healthy copy’s molecular instructions, boosting SERCA2 production to levels sufficient to correct the disease. The therapy is reversible, does not alter the genome, and is designed for topical delivery to affected skin.
The same platform can in principle be redirected to other diseases caused by the same type of genetic fault – opening the door to treatments for a broad range of currently incurable conditions.