Explore our grantees and awardees

Grant category: Research Grants

Year: 2025

Geography: Denmark

Pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa are commonly associated with non-healing and aggravated wounds, since they can colonize and invade host tissues, and many times cause life threatening conditions such as sepsis. Resistance to the available antibiotic therapies has been reported for both bacteria, and serious S. aureus skin infections are noted in both humans and animals. This project will investigate the ability of proteasome-derived defence peptides (PDDPs) – which can be naturally produced by our body – to protect against infection whilst promoting wound healing. It will also analyse the mechanisms by which PDDPs exert their effects. For this, different techniques (in vitro, ex vivo and molecular biology) will be used. For the ex vivo experiments, a wound dressing containing PDDPs will be developed with specific characteristics to allow PDDPs to target the pathogens whilst promoting wound healing.

Grant category: Research Grants

Year: 2025

Geography: Switzerland

Treatments for chronic inflammatory skin diseases rely on immunosuppression, which can increase infection risk and can fail to fully control disease. Keratinocytes of the epidermal barrier also actively drive inflammation. A protein family called the Gasdermins may play a key role in mediating release of inflammatory mediators from cells by forming pores in the cell membrane. At very high activity this kills the cell, but at lower activity these pores may allow controlled release of inflammatory signals, shaping communication between skin cells and immune cells.

This project will investigate:

1. How keratinocytes use Gasdermins for signaling without dying.

2. How chemical modifications fine-tune Gasdermin activity.

3. How these processes are altered in chronic inflammatory diseases, such as psoriasis and atopic dermatitis.

By identifying targets and biomarkers, this research could pave the way for new therapeutic avenues of exploration for inflammatory skin diseases.

Grant category: Research Grants

Year: 2025

Geography: Austria

Graft-versus-host disease (GVHD) is a serious complication of bone marrow transplantation, where donor immune cells attack the patient’s skin and other organs. In its different acute and chronic forms, GVHD can cause painful skin rashes, scarring, and long-term disability. Recent discoveries show that special long-lived immune cells, tissue-resident memory T cells (TRM), survive in the skin and drive this persistent inflammation. Current treatments do not specifically target these cells, which may explain why GVHD often flares up after treatment cessation. Our project will study skin samples from GVHD patients using cutting-edge technologies to uncover how TRM survive, reactivate, and interact with other cells in different GVHD stages. By identifying unique features and weaknesses of these cells, we aim to pave the way for new therapies that more effectively control chronic skin inflammation—improving care for GVHD patients and informing treatment of similar skin diseases.

Grant category: Research Grants

Year: 2025

Geography: United Kingdom

Discoid lupus (DLE) is an autoimmune disease giving rise to disfiguring facial lesions, with limited drug options. DLE lesions contain dense accumulations of B and T lymphocytes, but the reasons they develop, persist and recur is currently unknown. DLE’s systemic counterpart, SLE, affects many organs throughout the body. We can utilise the overlap between these related conditions to ask whether similar mechanisms might operate in both DLE and SLE. In systemic lupus, engagement between co-stimulatory molecules on the T and B cell surface drives B cell survival and produces a co-stimulatory effect. We will investigate whether a similar mechanism operates in lesion-resident B cells to promote lesion persistence and identify the cell surface molecules implicated. We will discover whether specific immune cofactors in the skin prevent cessation of the costimulatory signal. If successful, blocking co-stimulatory signals on B cells from DLE may provide the basis of future drug discovery.

Grant category: Research Grants

Year: 2025

Geography: Australia

Buruli ulcer is a neglected tropical skin disease caused by a bacterial infection and widespread across west and central Africa. Prompt diagnosis and correct antibiotic treatment is essential to prevent the serious disability and suffering that can arise with this disease. This project will develop a simple-to-use, rapid and low-cost diagnostic test for Buruli ulcer. This test can be used by health teams working in disadvantaged rural communities across Africa to provide prompt and correct treatment to reduce the suffering caused by this disease.

Grant category: Research Grants

Year: 2025

Geography: USA

Darier Disease (DD) is an incurable skin disease caused by pathogenic variants in one copy of a calcium pump called SERCA2, sometimes accompanied by neuropsychiatric symptoms and seizures. The disorder typically appears in teenagers and comes and goes in response to various forms of stress, resulting in painful lesions due to loss of epidermal tissue integrity, vulnerability to infection, and loss of self-esteem. Even though the underlying genetic basis of DD was discovered >25 years ago, treatments are still limited to non-specific drugs with distressing side effects, antibiotics, and behavior modification. We identified a unique vulnerability of DD cells caused by their failure to turn on a metabolic pathway that protects normal cells against stress. We aim to revive this protective pathway to restore normal metabolism in DD cells, and in so doing, enhance tissue integrity and the ability to repair DNA and prevent damage to the remaining good calcium pump.

Grant category: Research Grants

Year: 2025

Geography: United Kingdom

Fungal skin infections affect up to a quarter of people worldwide. They can also recur, spread and become life-threatening, especially in immunocompromised patients. This shows that our immune system does not always develop lasting and efficient protection. In particular, we don’t know why protective immune memory works so well against viruses but fails against fungi. Our project will study how special immune cells called T cells respond to fungal infections in the skin. By following patients with fungal skin infections over time, and comparing skin and blood samples, we will track how these immune cells are generated, maintained, or lost and what molecular weapons they use to fight the infection. We will use state-of-the-art and unique methodologies from our laboratory, allowing in-depth analysis of millions of T cells simultaneously at single-cell resolution. These insights could reveal new ways to strengthen our natural defenses and lay the foundation for future therapies.

Grant category: Research Grants

Year: 2025

Geography: United Kingdom

The normal healthy functions of our skin significantly decline with age, and these changes increase the risk of infection, chronic wounds, inflammatory diseases, and cancer. Therefore, understanding the biological mechanisms underlying skin ageing is essential to protect against age-related diseases and maintain healthy skin function. The aim of this project is to dissect the cellular, biochemical, and mechanical processes of skin ageing and to directly test how they impact key functions, including tissue homeostasis and immunity. We will take advantage of state-of-the-art imaging and genomic methods available within our institution to profile the ageing process, and advanced 3D culture models of human skin will be used to test key genes and biochemical pathways. The results will provide fundamental insights into human skin ageing, and over the long term, they have the potential to identify key therapeutic targets for counteracting or preventing age-related skin diseases.

Grant category: Research Grants

Year: 2025

Geography: USA

Most vaccines and textbook models assume that special immune messengers called cytokines (such as IL‑6 or interferon‑α) are needed to tell T cells what to become. These cytokines are normally triggered by adjuvants in vaccines or by the immune system sensing pathogens. Our new findings overturn this view. We discovered that Langerhans cells—immune sentinels in the skin—can trigger strong antibody responses even in the steady state, when those cytokines are absent. Instead of relying on inflammatory messengers, they use surface “grip” proteins (integrins) to fine‑tune the conversation with T cells. This cytokine‑independent pathway may explain how the immune system quietly learns from the skin microbiome and maintains balance, while errors in this mechanism could underlie autoantibody diseases such as pemphigus or lupus. Our first goal is to confirm these findings. Once established, they will guide new strategies for vaccines or treatments that prevent chronic inflammatory skin disease.

Grant category: Research Grants

Year: 2025

Geography: USA

Human skin pigmentation is highly variable among world populations and determines skin sensitivity to ultraviolet radiation, susceptibility to skin cancer, vitamin D production, and other outcomes. Much of this variability is determined by genetics. Using genetic analyses among diverse native Africans, we and our collaborators linked skin pigment variation with levels of expression of a gene called TMEM138. Inactivating mutations in TMEM138 or about 200 other genes cause developmental disorders called ciliopathies in which the primary cilium – a cell structure not known to impact pigmentation – fails to form properly. This proposal seeks to use cultured skin pigment cells called melanocytes and reconstituted human skin to better understand the molecular mechanisms by which TMEM138 specifically, and the primary cilium more generally, regulates pigment formation. Our study will provide new insights into skin pigment physiology and diseases and into how ciliopathy classes differ.