Bacteriophage therapeutics for Buruli ulcer
Grantee: Tim Stinear, Principal Research Fellow, University of Melbourne
Amount: DKK 1,081,850
Grant category: Serendipity Grants
Year: 2026
Geography: Australia
Buruli ulcer is a severe skin infection caused by a bacterium called Mycobacterium ulcerans. Treatment requires weeks of antibiotics and sometimes surgery, leaving patients with disability and scarring. While developing a new diagnostic test, we discovered a virus called 40C-del that infects and kills the Buruli ulcer bacterium very efficiently. This exciting finding suggests that 40C-del might be developed into a new treatment. In this project, we will investigate exactly how 40C-del attacks and destroys the bacterium and test whether combining it with another virus (D29) improves effectiveness. We will also examine whether the bacterium can become resistant and whether the virus remains stable under conditions relevant to future medical use. By the end of the project, we will know whether 40C-del can become a future therapy for Buruli ulcer. This serendipitous discovery could ultimately lead to safer, more targeted treatments for people affected by this neglected tropical disease.
Beyond Hormones: Sex-Biased Gene Regulation in Human Skin Wound Healing
Grantee: Ning Xu Landén, Associate Professor, Karolinska Institutet
Amount: DKK 3,998,400
Grant category: Serendipity Grants
Year: 2026
Geography: Sweden
Wounds do not always heal in the same way in everyone. Men and women can differ in how their skin repairs itself, but most research has focused on the effects of sex hormones. Our recent work suggests that the difference may go deeper: some genes that change during wound healing are also expressed differently in male and female skin. This project will explore whether male and female wounds use different molecular programs to repair damaged tissue. We will study human skin wounds using advanced technologies that allow us to analyze thousands of individual cells and see where important genes are active in the tissue. We will also study skin samples from transgender donors receiving hormone treatment, which may help us separate the effects of hormones from more intrinsic biological differences. Finally, we will test selected genes in human skin cell and wound models. This work may reveal new mechanisms of wound healing and support more precise treatments for chronic, non-healing wounds.
Memory ILC2s link chronic allergic inflammation to haematopoietic ageing
Grantee: Itziar Martinez Gonzalez, Assistant professor and Group Leader, Karolinska Institutet
Amount: DKK 3,995,250
Grant category: Serendipity Grants
Year: 2026
Geography: Sweden
Allergic diseases such as atopic dermatitis and asthma often start early in life and can flare repeatedly. They are also linked to health problems outside the skin and lungs, including increased risk of blood clotting and cardiovascular disease, but the reasons are poorly understood. This project asks whether long-lasting “memory” immune cells involved in allergy, called ILC2s, can send signals to the bone marrow and change how blood cells are produced. We will use established mouse models of allergic inflammation together with advanced cell analysis, gene expression studies and functional tests of blood-forming stem cells. We will also compare key findings with human samples. By revealing how allergic inflammation affects the bone marrow, the project may uncover new explanations for allergy-associated comorbidities and identify future strategies to prevent long-term complications of allergic disease.
Does Sensory-Sympathetic Rewiring Drive Cutaneous Neuropathy?
Grantee: Clare Bennett, Professor of Cellular Immunology, University College London
Amount: DKK 2,889,362
Grant category: Serendipity Grants
Year: 2026
Geography: United Kingdom
The skin is an important sensory organ, with nerve endings extending into its outer layer (the epidermis), to detect heat, cold and harmful stimuli. In some skin diseases and during cancer treatments, these nerves are damaged and withdraw from the epidermis. Instead of causing numbness, this often leads to chronic, difficult-to-treat pain; in cancer patients, it can limit treatment. But why this happens is not fully understood. We are studying how immune cells in the skin interact with nerve endings. In our models, we see nerve loss similar to patients. Unexpectedly, when the nerves try to regrow, we have discovered that they follow the paths made by other types of nerves (sympathetic nerves) and end up in the wrong place, near hair follicles rather than in the epidermis. We think this misdirected growth causes nerves to behave as if they are detecting danger, triggering pain. By understanding this process, we aim to find ways to guide nerves correctly and reduce chronic pain.
A Non-Invasive Genomic and Transcriptomic Decision-Assist Tool for Suspected Subungual Melanoma
Grantee: Beth McLellan, Professor and Chief, Albert Einstein College of Medicine
Amount: DKK 3,999,656
Grant category: Serendipity Grants
Year: 2026
Geography: USA
While studying skin bacteria, we made a surprising discovery: simple, painless nail clippings contain readable human genetic messages (mRNA). Scientists previously believed these delicate messages were completely destroyed as nail cells harden and die. This unexpected finding could revolutionize how we diagnose subungual melanoma, a deadly skin cancer growing under the nail. Currently, diagnosing this cancer requires a painful surgical biopsy of the nail bed, risking permanent deformity. Our discovery suggests we might detect this cancer, and understand its deeper biology, just by analyzing a painless clipping. To investigate this, we will collect nail clippings from patients with harmless dark spots and those with confirmed nail cancer. Using advanced technology, we will read the surviving genetic messages to identify a “signature” of the cancer. We will also explore if these clippings reveal how the tumor interacts with the immune system, paving the way for pain-free diagnostics.
Nasal microbiota as a novel axis for skin immune regulation
Grantee: Yiyin Chen, Assistant Professor (MIT), Core Institute Member (Broad Institute)
Amount: DKK 3,999,997
Grant category: Serendipity Grants
Year: 2026
Geography: USA
We aim to understand how skin inflammation is suppressed by a surprising site: the nose. This proposal is motivated by two unexpected discoveries during our prior Leo-funded work. First, we found that some bacteria generate large immune responses when they colonize the nose peacefully, even when there is no evidence of infection. Second, we found that these nasal bacteria suppress the immune response in the skin, even though the skin is 100x larger than the nose. Therefore, we hypothesize that the nose is an overlooked site of immune regulation for the skin. We now aim to understand the molecular details of this nose-skin immune suppression. We also plan to study how nose-skin immune suppression changes our risk of eczema, psoriasis, infection, and cancer. Overall, we hope to understand how the bacteria that naturally colonize our nose regulate skin health and use these insights to develop new therapies for skin inflammation.