The 2025 Gordon Research Conference on Barrier Function of Mammalian Skin
Grantee: Associate Professor Pankaj Karande, Rensselaer Polytechnic Institute, US on behalf of Gordon Research Conferences, US
Amount: DKK 495,729
Grant category: Research Networking
Year: 2024
Geography: USA
The skin barrier is the first defense against the external environment, and barrier disruption plays a key role in skin and systemic diseases that impact millions of people. The main purpose of the GRC Barrier Function of Mammalian Skin conference is to bring together young investigators and prominent leaders to present the latest developments in skin barrier research.
The 2025 conference, Technologies and platforms for understanding, modelling and intervening in skin barrier function and disorders, will bring together researchers, scientists, engineers, and clinicians involved in research related to skin health and disease. Diverse areas of science will be covered, including cell biology and pathology, microbiology, environmental sciences, bioengineering, biophysics, physical chemistry, and drug delivery.
The meeting will be held August 10-15, 2025.
The LEO Foundation has provided support for the previous Gordon Research Conferences.
The 2025 Gordon Research Conference on Epithelial Differentiation and Keratinization (GRC-EDK)
Grantee: Associate Professor Maria Kasper, Karolinska Institutet, SE on behalf of Gordon Research Conferences, USA
Amount: DKK 319,712
Grant category: Research Networking
Year: 2024
Geography: USA
The Gordon Research Conference on Epithelial Differentiation and Keratinization (GRC-EDK) has been the premier international meeting in skin biology since 1979. The 2025 GRC-EDK meeting is called Epithelial Development, Aging, Disease and Regeneration Across Cells and System and brings together speakers at the forefront of areas including skin immunity, tissue sensing and crosstalk, genomics and epigenomics, aging, regeneration, and novel technologies to drive therapy. The meeting will foster intense interactions at the interphase of these different disciplines and promote discussion to discover synergies and novel therapeutic prospects to advance the field as a whole.
The event will take place May 31-June 1, 2025.
The LEO Foundation has provided support for the three previous Gordon Research Conferences.
Wearable Sensor to Enhance Diagnostics and Health Equity in Allergic Contact Dermatitis
Grantee: Aydogan Ozcan, Professor, The Regents of the University of California, Los Angeles, USA
Amount: DKK 2,854,181
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Aydogan Ozcan’s project explores a potential alternative to the current diagnostic standard in allergic contact dermatitis (ACD) —patch testing —which has remained largely unchanged since its development over a century ago. It seeks to transform the diagnosis of ACD by developing a novel wearable sensor capable of remote monitoring and early detection. The sensor will be designed to measure changes in the skin’s optical properties, offering a more efficient, convenient, and comfortable alternative to the traditional method of patch testing. Aydogan Ozcan’s project includes the creation of skin phantom models’ representative of diverse skin tones to rigorously test the wearable sensor, followed by a phased human study.
The results of the project could enable more convenient, equitable, and cost-effective diagnosis in ACD, thereby improving patient outcomes. Additionally, this technology holds the potential to be adapted for the monitoring of other skin conditions, representing a significant advancement in the field of dermatology.
Primary cilia: a novel target for skin fibrosis
Grantee: Maria Teves, Assistant Professor, Virginia Commonwealth University, USA
Amount: DKK 3,914,945
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Maria Teves’ project explores mechanisms behind formation of dermal fibrosis, which is a hallmark of several skin disorders, including systemic sclerosis (SSc). Despite the identification of various contributing factors, the precise molecular mechanisms underlying skin fibrosis in SSc remain poorly understood and there is no effective treatment. In order to uncover these mechanisms and develop new therapeutic strategies, the project focuses on primary cilia (PC), which are specialized solitary cellular organelles involved in molecular signaling. Recently, Maria Teves and her research group discovered links between altered PC to SSc pathophysiology, revealing significant alterations in PC and PC-associated gene expression in skin biopsies from SSc patients. Furthermore, it was found that profibrotic signaling can be triggered both in vivo and in vitro by the genetic ablation of PC-associated genes or by pharmacological agents that damage PC. Building on this critical evidence, the project will test the hypothesis that PC represent novel therapeutic targets for SSc skin fibrosis. A comprehensive approach is proposed to define molecular contributions of PC to the pathogenesis of skin fibrosis and assess the potential of PC-targeted therapies for mitigating fibrotic phenotypes.
Maria Teves’ experiments may lay the groundwork for advanced understanding and possibly treatment and future clinical advances for people suffering from fibrotic skin conditions.
Identifying new, molecularly-targeted treatments for rosacea
Grantee: Anand Ganesan, Professor, The Regents of the University of California Irvine, USA
Amount: DKK 4,000,000
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Anand Ganesan’s project explores the activation of the innate immune system in rosacea, a chronic skin condition which affects 5% of the world’s population. Rosacea skin has an increased number of blood vessels, which can be induced by the naturally occurring anti-microbial peptide cathelicidin, which is produced by keratinocytes in rosacea skin. While treatment targets and new pharmacotherapies for rosacea have been identified, this knowledge has not yet been translated into new rosacea therapies. RhoJ, a member of the CDC42 GTPase family, plays a critical role in angiogenesis (formation of new blood vessels) in skin and other organs, and RhoJ knockout mice have decreased number of blood vessels in the skin as compared to wild type animals. Anand Ganesan and the research group has discovered a new class of small molecules that inhibit CDC42 GTPase signaling, which prevents vessel accumulation in the skin and colon through a RhoJ-dependent mechanism and also blocks the vascularization of human organoids. Anand Ganesan’s project couples’ single cell and spatial transcriptomics approaches (i.e., analyses of how genes are expressed in individual cells as well as throughout a tissue) with advanced bioinformatics to identify vessel inducing signals in tissue. The research plan includes 1) coupling single cell and spatial transcriptomics with advanced bioinformatics to identify rosacea inducing signals; 2) quantifying vascular changes in rosacea in mice and human model systems; and 3) testing the efficacy of CDC42 inhibitors at blocking cathelicidin-induced angiogenesis.
The project aims to identify new drug targets and test the efficacy of new treatments for rosacea.
Determining the Impacts of Testosterone on S. aureus-induced skin Damage in Atopic Dermatitis
Grantee: Tamia Harris-Tryon, Associate Professor, UT Southwestern Medical Center, USA
Amount: DKK 2,852,706
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Tamia Harris-Tryon’s study explores atopic dermatitis (AD) which affects seven percent of adults and twenty percent of children. AD has the highest impact on patient quality of life among skin disorders. The pathogenesis of AD is incompletely understood, and there is an increasing appreciation for the contributions of the microbiome. During AD flares, Staphylococcus aureus expands and exacerbates inflammatory responses and skin damage. While S. aureus dominates the skin microbiome in AD, the mechanisms that drive bacterial expansion during inflammation remain unclear. This question is important because skin breakdown in AD is aggravated by S. aureus toxins. S. aureus exotoxins have been shown to stimulate skin inflammation. Tamia Harris-Tryon’s project will test the central hypothesis that testosterone promotes S. aureus-induced skin damage and inflammation in AD as well as investigate how testosterone stimulates S. aureus-induced skin damage in culture and in mouse models. These experiments will also make use of genetically engineered mice with reduced testosterone production in the skin. This approach will reliably determine how testosterone regulates S. aureus-induced skin damage and inflammation.
The results of Tamia Harris-Tryon’s project may reliably determine how testosterone regulates S. aureus-induced skin damage and inflammation.
Viral hijacking of embryonic signaling pathways in trichodysplasia spinulosa
Grantee: Andrzej Dlugosz, Professor, University of Michigan, USA
Amount: DKK 3,985,000
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Andrzej Dlugosz’s project explores how a skin-associated virus called TSPyV can cause a striking hair follicle disorder called trichodysplasia spinulosa. In patients affected by this condition hair follicles on the face and ears are enlarged, structurally abnormal, filled with TSPyV viral particles, and produce spikes instead of hairs. To understand how TSPyV disrupts hair follicle biology Andrzej Dlugosz and his group created genetically engineered mice that express TSPyV viral proteins in skin. These mice produced enlarged and abnormal-appearing follicles and developed follicle-like structures in hairless areas, suggesting that TSPyV can somehow reprogram skin to drive growth of hair follicles which are needed for large-scale virus production. In keeping with this concept, one of the TSPyV viral proteins triggers abnormal activation of an important molecular signal that regulates formation and maturation of hair follicles. The studies will examine hair follicles in trichodysplasia spinulosa using powerful new molecular technologies to better understand the alterations in behavior and maturation of follicle cell types in this disease. They will also investigate how a specific TSPyV protein hijacks an important hair follicle signaling pathway, contributing to the profound changes seen in the skin of trichodysplasia spinulosa patients.
The results of the project have the potential to yield new insights into the regulation of molecular signals controlling formation and growth of hair follicles, based on findings from studying this rare condition.
Ex Vivo Culturing of the Human Skin Microbiome
Grantee: Beth McLellan, Professor, Albert Einstein College of Medicine, USA
Amount: DKK 4,054,452
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Beth McLellan’s project, in collaboration with co-PI and Kosaku Shinoda, explores the functional interactions of live or viable bacteria within the skin microbial community, and their implications in skin disease. The project aims to develop a robust ex vivo model, Skin Microbiome in a Test tube (SMT), to study the dynamic biochemical activity of the viable skin microbiome. Preliminary data indicate that the prototype version of the SMT system (v1) is capable of preserving the diversity of skin bacteria ex vivo. The aims are to (1) refine SMT using Propidium Monoazide (PMA) sequencing to exclusively replicate the viable microbiome and (2) investigate the impact of skin microenvironmental factors (e.g., moisture, sebum levels, and skin breakdown) on the composition and biochemical activity of the viable microbiome, using data from non-invasive sensors at multiple skin sites.
With the generation of the improved version of the SMT (v2), the project hopes to create an innovative platform for functional skin microbiome studies, drug screening and pharmacokinetic modeling with an emphasis on microbial viability leading to individualized treatment strategies based on microbiome community profiles. SMT will serve as a foundation for identifying biomarkers, developing microbiome-based therapies, and improving pharmacokinetic predictions.
Defining how skin microbial communities shape T cell function using a novel antigen-tracking technology
Grantee: Erin Chen, Assistant Professor, Broad Institute of MIT and Harvard, USA
Amount: DKK 3,929,293
Grant category: Research Grants in open competition
Year: 2024
Geography: USA
Erin Chen’s project aims to address the fundamental question: how do we translate the composition of our body’s colonizing microbes (our microbiome) into insight about immune function? Commensal bacteria (commonly known as just “commensals”) colonize our skin, over our entire lives, and generate the vast majority of microbe-host encounters, with largely unknown consequences. Erin Chen’s project focuses on commensals’ interactions with T cells because these cells critically impact many aspects of health and disease. Unlike infections, where a single pathogen invades into the tissue, commensals colonize within complex communities and communicate to the host immune system across an intact skin barrier. How the immune system decodes signals from each member of this community is unknown. Erin Chen and her team will address this by colonizing mice with defined communities of commensals and tracking the commensal-derived antigens along with the strain-specific T cells. To do this, they will develop novel methods to detect commensal-derived antigens within the host tissue, at high resolution. By varying the abundance and composition of community members, they aim to discover novel antagonistic, synergistic, and emergent properties of commensal-specific T cells. This work will provide visibility into a currently invisible process: how a lifetime of commensals on our skin are constantly sculpting our T cell function, which ultimately impacts our susceptibility to infections, autoimmunity, and cancer.
How innervation regulates regeneration and scarring responses
Grantee: Ya-Chieh Hsu, Professor, Harvard University
Amount: DKK 4,000,000
Grant category: Serendipity Grants
Year: 2024
Geography: USA
Ya-Chieh Hsu’s project investigates the mechanisms behind the unexpected observation that wound healing slows upon increased innervation of the surrounding tissue.
During testing of a virus-based tool designed to genetically manipulate skin cells Ya-Chieh Hsu and her team serendipitously discovered that increased innervation at a wound site slows healing and leads to increased scarring. This discovery suggests that wound-induced hyper-innervation may be important in driving scarring and fibrosis.