Explore our grantees and awardees

Grant category: Research Networking

Year: 2025

Geography: USA

The Vulvar Dermatology Research Consortium (VDRC) will host a special two-hour Young Investigators Symposium as part of its Annual Meeting on Thursday, March 26th, 2026, in Denver, Colorado. This event is designed for medical students, residents, dermatologists, and other physicians, patients, industry partners, and scientists interested in vulvar skin problems. Participants will share research, gain insights from vulvar skin experts, and connect with others in the field. Ultimately, this event will facilitate collaboration on vulvar skin health research, to promote improved outcomes for people living with vulvar skin conditions.

Grant category: Research Networking

Year: 2025

Geography: USA

The 2026 Epithelial Stem Cells and Niches Gordon Research Conference and Seminar will be held August 22–28, 2026, in Spain. It will bring skin researchers together with leading stem cell biologists working on other organ systems to cross-pollinate ideas and technologies. Interactions and collaborations that emerge from this conference will accelerate discovery in the skin and support the development of new cures for skin diseases. The meeting includes a dedicated session for trainees and will support early-career researchers through travel grants, mentoring, and short talk opportunities.

Grant category: Research Grants

Year: 2025

Geography: USA

Psoriasis is a prevalent chronic autoimmune skin disease considered a major global health issue, driven by overactive immune signals, especially those from interleukins IL-17 and IL-23 pathways. Current therapies, mainly injectable antibody drugs, can be highly effective but are costly, requiring medical administration, and remain in patients for weeks, causing long-term safety concerns. Our project aims to create a new class of smaller molecules that work like antibodies but act rapidly and will ultimately be taken orally. Using discoveries from our lab on CDR-H3-mimicking small molecules—structures inspired by the critical binding loops of antibodies—we can precisely block interactions that trigger IL-17 and IL-23 activity. This innovative technology could deliver powerful anti-psoriasis molecules that are easier to dose, more affordable, and potentially safer for long-term care. Success will open the door to a new generation of small-molecule therapies for autoimmune diseases.

Grant category: Research Grants

Year: 2025

Geography: USA

Pyoderma gangrenosum (PG) is a rare and very painful skin disease that causes rapidly enlarging ulcers which can destroy tissue and severely impair quality of life. It is often misdiagnosed because there are no specific tests and its ulcers resemble other chronic wounds, leading to delays, wrong treatments, and prolonged suffering. PG is frequently linked to other serious conditions such as inflammatory bowel disease or arthritis. Current therapies mainly suppress the immune system but are often ineffective, and no approved targeted treatment exists. Our project will apply cutting-edge technologies to study genes, proteins, and single cells in PG skin samples and compare them with other types of ulcers. By defining unique “molecular fingerprints” of PG, we aim to develop the first reliable diagnostic test, uncover disease subtypes, and identify new drug targets. This will allow earlier diagnosis, guide personalized therapy choices, and ultimately transform patient care.

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: 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.

Grant category: Research Grants

Year: 2025

Geography: USA

Immunotherapy has transformed cancer treatment, helping the body’s immune system attack tumors. Unfortunately, these powerful drugs often cause side effects when the immune system also attacks healthy tissues. The skin is one of the most commonly affected organs, leading to rashes and other painful conditions that can force patients to stop life-saving therapy. Our project aims to understand why this happens. We recently discovered that certain immune cells, called CD8 T cells, are activated by bacteria living on the skin and then attack healthy skin cells during treatment. We will study how these bacteria and immune cells interact and test new ways to prevent this process. By uncovering how microbes trigger skin damage, our research could pave the way for safer cancer immunotherapies, helping patients stay on treatment longer while avoiding harmful side effects.

Grant category: Serendipity Grants

Year: 2025

Geography: USA

Organisms are continuously bathed in a rich milieu of olfactory compounds. Defined by their ability to elicit the sense of smell, these molecules, and the receptors that sense them, have profound biological importance. Humans have hundreds of olfactory receptors, but paradoxically these are often expressed outside of the nasal cavity and on immune cells. Their function in these contexts is almost entirely unknown. The serendipitous finding illustrates that: a) olfactory receptors are enriched in inflamed skin and on lesion infiltrating lymphocytes; and b) odorants directly modulate lymphocyte function. Understanding the role and molecular mechanisms of these pathways in inflammation may open new avenues for treating skin disease with promise for targeted topical approaches.

To explore this serendipitous finding, the research project will combine in vivo models of skin inflammation with expertise in multiomic analyses of hidradenitis suppurativa (HS) and pyoderma gangrenosum (PG) patient tissues. The study will determine if exposure to olfactory molecules modulates skin inflammation in vivo, functionally dissect immune cell intrinsic olfactory signaling, and identify signatures of pathway activity in HS and PG.

This work will provide insight into the fundamental biology of immune-olfactory signaling and determine if there is functional relevance for skin inflammation. The project will also test the implications for HS and PG, where novel therapeutic approaches are urgently needed.

Grant category: Serendipity Grants

Year: 2025

Geography: USA

Hailey-Hailey disease (HHD) is a rare genetic disorder causing recurrent skin blistering and infections. Despite linkage to heterozygous (HET) mutations depleting the SPCA1 Golgi calcium pump 25 years ago, HHD lacks proven therapies. Cory Simpson’s LEO-funded research using in vitro HHD models led to two serendipitous discoveries that fuel this grant: (1) a JNK inhibitor intended as a negative control markedly strengthened adhesion among HET keratinocytes; (2) this led them to re-analyze RNAseq data, which revealed an overlooked aberration that may make HHD patients susceptible to pathogens like herpes simplex virus (HSV). Previously they focused on upregulated pathways amenable to drug inhibition; re-examining downregulated genes in HET cells, they found suppression of type 1 interferon (IFN) signaling. These data support their hypothesis that stress-induced JNK activation upon Golgi protein misfolding in HET keratinocytes weakens cell junctions to cause blistering and dampens IFN responses, facilitating viral infection.

To test these ideas, Cory Simpson required new tools and collaborators in immunology and virology, who provided biosensors to visualize and quantify JNK and type 1 IFN activity along with GFP-tagged HSV to infect the HHD models.

The planned work will test if modulating JNK or type 1 IFN in the HHD model can bolster epidermal integrity and suppress viral infection. Thus, the project has potential to directly impact treatment of patients with this orphan disease.