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.
HLA-informed modelling of tissue-relevant TCR and epitopes driving SJS/TEN.
Grantee: Andrew Gibson, Research Laboratory Lead, Murdoch University, Australia
Amount: DKK 3,039,471
Grant category: Research Grants
Year: 2026
Geography: Australia
Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a life-threatening skin reaction to certain drugs, driven by immune cells called CD8+ T cells. Our research aims to uncover why only some people are at risk by studying how specific immune receptors (TCRs) and genetic markers (HLA) interact with drugs to activate CD8+ T-cells in the skin. We have found that certain HLA markers linked to SJS/TEN share structural features and that drug-reactive TCRs come from pre-existing immune cells in the skin from past viral infections. This suggests drug reactions may involve crosstalk between drug and viral signals. We will now model these interactions in (i) patients to predict dangerous drug-HLA combinations for safer drug treatment and (ii) naïve immune cells from healthy donors to model early immune reactions and predict ‘high-risk’ drugs for safer drug development. This work could lead to new clinical and preclinical strategies to prevent SJS/TEN and reduce its global impact.