Research Grants

Grant category: Research Grants

Year: 2026

Geography: USA

Vitiligo is a skin condition caused by the progressive loss of pigment cells, leading to white patches on the skin. The condition becomes active and detectable at a cellular level long before visible skin changes are observed. However, current methods to detect such cellular-level damage require invasive biopsies. Our project will enable preventative treatments and monitoring using a noninvasive imaging tool. By combining optical imaging with spatial omics, we will develop the first cellular-level map of vitiligo without the need for biopsies. This innovative tool will use artificial intelligence to identify specific cell types and monitor disease progression in real time. This approach promises to enhance early detection and treatment of vitiligo and has potential applications for various other skin conditions, such as inflammation and cancer. Ultimately, this could lead to more personalized and effective treatments, improving patient outcomes and accelerating drug development.

Grant category: Research Grants

Year: 2026

Geography: USA

Cutaneous lupus erythematosus (CLE) is a skin disease in which sunlight, instead of calming the immune system, triggers painful and damaging inflammation. This unusual reaction is poorly understood, making it difficult to prevent disease flares.
Our research has identified a group of immune cells in the skin that become highly inflammatory after sun exposure and drive tissue damage. However, the signal that activates these cells remains unknown.
We propose that a stress-related protein released by skin cells after UV exposure acts as a trigger that turns these immune cells into harmful inflammatory cells. To test this, we will study human skin samples and examine how blocking or adding this signal affects immune activation.
Understanding this mechanism could lead to new strategies to prevent sun-induced flares in lupus and related diseases.

Grant category: Research Grants

Year: 2026

Geography: USA

Demodex mites usually live harmlessly and at low levels in facial hair follicles and sebaceous glands. Still, in some people, they become overabundant and are linked to chronic inflammatory skin diseases such as rosacea. The key problem is understanding why the immune system sometimes tolerates these mites and other times triggers persistent inflammation. Our research aims to identify the molecular “switch” that determines this outcome. Using a mouse model of Demodex infection and novel Demodex-keratinocyte co-culture systems, we discovered that a signaling pathway involving IL-36 and gasdermin proteins activates protective type 2 immune cells that control mites. However, when dysregulated, this same pathway may drive excessive inflammation. By defining how skin cells sense Demodex and regulate immune responses, we aim to uncover new, targeted treatments for rosacea and other inflammatory skin conditions linked to microbial imbalance.

Grant category: Research Grants

Year: 2026

Geography: USA

Inflammatory skin diseases can be more common and severe in people of African ancestry, but the biological reasons are unknown. Our work shows that healthy skin from individuals of African ancestry has elevated interleukin 1 (IL 1) signaling, and that a specific DNA region regulating this pathway carries a variant with higher frequency among individuals of African ancestry. This project will provide mechanistic understanding of how this genetic difference changes the way skin cells sense and respond to IL 1 signaling. We will edit the variant in human skin cells and read out the effects at single cell resolution, both in the lab and in donated skin samples. By revealing how inherited differences in skin regulation drive susceptibility to inflammation, the project will lay the groundwork for ancestry aware, more precise treatments that better control disease and help reduce inequities in skin health.

Grant category: Research Grants

Year: 2026

Geography: USA

Many skin conditions like eczema, psoriasis, and hair loss are caused by an overactive immune system. Two types of medications, PDE4 inhibitors and JAK inhibitors, can calm this immune response, but each has drawbacks. PDE4 inhibitors can cause nausea and headaches because they enter the brain, while JAK inhibitors may increase infection risk. Our research asks: what if we combine both medications at lower doses? This could provide better, synergistic treatment with fewer side effects. Building on our previous work understanding how these drugs work at the molecular level, we will use artificial intelligence and computer simulations to: (1) predict which drug modifications prevent brain entry; (2) find the best drug combinations; and (3) design new, safer medications. We expect this research could lead to more effective treatments for many people with inflammatory skin diseases, with fewer side effects than current options, improving the patient standard of care.

Grant category: Research Grants

Year: 2026

Geography: USA

Bullous pemphigoid (BP) is a skin disease in which the immune system attacks a protein called BP180 that helps hold the layers of the skin together. This causes itching, inflammation, and blistering, mainly in older adults. BP is becoming more common as the population ages, and it is still associated with a relatively high risk of death, showing the need for better treatments.

Research has been limited because current BP models are not close to real human skin. In this project, we will use human stem cells to grow miniature skin tissues, called skin organoids, that mimic key features of human skin. We will expose these organoids to disease-causing BP antibodies to study how skin damage begins, how the skin becomes fragile, and how the immune reaction develops. This work will improve our understanding of BP, reveal possible treatment targets, and create a new human model for developing and testing future therapies.

Grant category: Research Grants

Year: 2026

Geography: USA

Bullous pemphigoid (BP) is a serious blistering skin disease usually treated with long courses of steroids, which can cause major side effects. Despite advances in treatment, therapy for acute disease still relies heavily on prolonged high-dose oral corticosteroids. We found that a molecule called VEGF-A—known for driving inflammation—is much higher in the blood, and skin of people with BP. VEGF-A also rises alongside many other inflammatory signals. Early experiments in mice show that blocking VEGF-A can make the disease noticeably less severe. This project will test whether targeting VEGF-A can quickly reduce skin involvement in relevant models of pemphigoid. We will also study whether VEGF-A made specifically by skin cells is a key trigger of inflammation, and whether blocking VEGF-A in the skin (including with topical treatments) can help. The goal is to determine if VEGF-A could be a new, fast-acting, steroid-sparing treatment for BP.

Grant category: Research Grants

Year: 2026

Geography: USA

Atopic dermatitis (AD) is a chronic condition characterized by a weakened skin barrier, inflammation, and itch. Existing treatments mainly focus on relieving inflammation without directly addressing the skin barrier’s impairment. Our goal is to develop a topical treatment for AD that strengthens the skin barrier while reducing inflammation, an approach not previously explored. We recently discovered that a protein named RET is hyperactivated in AD, and inhibiting RET topically has shown promising results in enhancing the skin barrier and reducing inflammation. We hypothesize that topical RET inhibitors could effectively prevent and/or treat AD. Our proposal seeks to investigate how RET modulates skin barrier function and demonstrate the therapeutic effectiveness of topical RET inhibition using an established animal model that mimics human AD. This research is essential to fully explore RET as a therapeutic target in AD and advance the development of RET inhibitors for this condition.

Grant category: Research Grants

Year: 2026

Geography: USA

Behçet’s disease is a chronic inflammatory condition that can affects the skin, mucous membranes, and multiple organs, and can be difficult to diagnose and treat. The immune mechanisms driving this disease are not well understood. Our research shows that a specific group of immune cells, called monocytes, are abnormally activated in Behçet’s disease, largely due to the action of interferon-gamma. This activation changes with treatment and differs across disease types, such as eye or blood vessel involvement. In this study, we will identify the signals that cause and sustain this abnormal immune response, develop blood-based markers to track disease activity and remission, and test whether blocking key inflammatory pathways can restore normal immune cell function. This work aims to improve disease monitoring and support the development of more targeted and effective treatments for patients with Behçet’s disease.