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.
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.