Explore our grantees and awardees

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.

Grant category: Research Networking

Year: 2025

Geography: USA

The 18th International Workshop of Langerhans Cells and Related Myeloid Cells in the Skin will take place on September 3–5, 2025, at Washington University in St. Louis. This global scientific meeting brings together researchers to explore the biology and interaction of immune cells in the skin – how they protect us, how they contribute to diseases like eczema, psoriasis, and skin cancer, and how they can be targeted for new treatments. The workshop fosters discovery, collaboration, and innovation in skin science, with talks by leading scientists, and early-career researchers, males and females from around the world. Read more information here.

Grant category: Research Networking

Year: 2025

Geography: USA

The 72nd Annual Montagna Symposium will be held October 16th-20th on the Oregon Coast. The symposium will focus on emerging paradigms in personalized medicine.

Population studies have raised questions about why individuals do not respond to established therapies. Patients are individuals with personalized social, behavioral, and genetic determinants, but knowledge gaps exist regarding how these determinants influence diagnosis and treatment of cutaneous diseases. The goal is to highlight emerging avenues of investigation and streamline their incorporation into clinical medicine.

This event is designed for senior and junior level leaders in the field: scientists, dermatology clinicians, clinical, translational and basic science researchers, and trainees. The format includes lectures, discussions, and many networking opportunities which enable interaction between new and established scientists and dermatologists. Visit the website for the program and registration.

Grant category: Research Grants

Year: 2025

Geography: USA

Pyoderma gangrenosum (PG) is a rare skin disease. Patients with PG have defects in their skin wound healing responses. Even minor injuries and cuts to the skin can form large chronic ulcers. PG ulcers are enriched with neutrophils, an immune cell type that plays a vital role in skin wound healing. Typically, neutrophils travel to the skin right after an injury, perform their tasks, and leave within a period of 3 days. Samreen Jatana wants to understand why PG neutrophils don’t perform their regular tasks and impair wound healing in skin. Samreen Jatana and her colleagues analyzed peripheral blood from patients with PG and identified a type of neutrophil in circulation with features of immature neutrophils that typically live in the bone marrow. They anticipate that this neutrophil subset cannot utilize energy properly and might be exhausted to perform its function. In this project, they will study this neutrophil subset to understand if it can be targeted therapeutically to treat PG.

Grant category: Research Grants

Year: 2025

Geography: USA

Keloids are raised, inflamed scars that grow beyond the original wound, often becoming painful and disfiguring. They disproportionately affect African American, Hispanic/Latino, and Asian individuals, yet the biological reasons behind their formation remain unclear. Current treatments are limited, with high recurrence rates. George Agak’s research aims to uncover the molecular drivers of keloids by studying skin cells from keloid-prone individuals at the single-cell level. George Agak and his team focus on a key signaling pathway, the ACE-ASPN axis, which appears to promote inflammation and excessive scar formation. By using cutting-edge technologies like scRNA-seq, spatial-seq and advanced machine-learning tools, they will map how keloids develop across diverse skin types. Additionally, they will test whether angiotensin receptor blockers (ARBs)—drugs already used for high blood pressure—can reduce keloid growth. The goal is to identify targeted treatments, leading to personalized therapies for those most affected.

Grant category: Research Grants

Year: 2025

Geography: USA

Sclerodermatous chronic graft-versus-host disease is a common, debilitating side effect that can develop in patients who have undergone hematopoietic stem cell transplantation for blood cancer. It is challenging to treat and usually requires medications that suppress the immune system. One of the biggest challenges in treating patients with cGVHD is the lack of an accurate informative way for doctors to know if the skin is responding to therapy or is getting worse. In this project, Adela Cardones will use novel ultrasound technologies to measure changes in skin stiffness among cGVHD patients over a 1-year period. Adela Cardona and her team will compare this with using traditional clinical assessment, patient reported symptoms, and blood and skin markers of inflammation. If successful, this will allow them to better detect worsening or improvement of skin thickening and stiffness. This will ultimately lead to better care of patients and allow discovery of better treatments.