Summer 2025 Gina M. Finzi Fellows
The Lupus Foundation of America awarded seven individuals to receive the 2025 Gina M. Finzi Memorial Student Summer Fellowship Award.
The Finzi Fellows are spending their summer conducting research in areas that are critical to moving the lupus research field forward. The Finzi Fellows are mentored by an established lupus investigator throughout the duration of their summer research program. The results of research by the awardees will contribute to new therapies, prevention strategies and educational interventions to better understand, detect and treat people with lupus.
The 2025 Gina M. Finzi Memorial Student Summer fellows are:
Grace Crossland
Mentor: Sladjana Skopelja-Gardner, PhD
Institution: Dartmouth College, Geisel School of Medicine
Project Title: Defining the role of mucosal-associated invariant T (MAIT) cells in cutaneous lupus erythematosus
Project Summary: Cutaneous lupus (CLE) affects >80% of all lupus patients. The skin lesions that result from CLE are painful, disfiguring, and affect the mental health and quality of life of these patients. Mucosal-associated invariant T (MAIT) cells are a type of immune cell that is important for protecting and repairing tissues at barrier sites, including the skin. These protective MAIT cells are reduced in the skin of CLE patients compared to healthy individuals, which may contribute to the development of skin disease in lupus.
Using mouse models of CLE, we have shown that by directly stimulating the few MAIT cells that are in CLE skin, we can expand these cells and drive healing of skin lesions. When we do this, we have also observed increases in another important immunosuppressive cell type, regulatory T cells (Treg). Given the striking improvement in skin disease that is seen with MAIT cell expansion and their potential relationship with Treg, it is critical that we understand how MAIT cells change upon stimulation and how they may be driving skin healing.
In my proposed studies, I will carefully evaluate MAIT cells in the skin of both healthy and CLE mouse models before and after stimulation to understand how their function changes in healthy versus lupus states. I will also use other immunologic approaches to test the contribution of MAIT cell-driven Treg to the resolution of skin lesions in the CLE mouse model. The findings from these proposed studies will provide critical information about potential mechanisms of skin protection that are reduced or dysfunctional in lupus and how we can modulate these pathways to treat disease.
Vanessa Estrada
Mentor: James J. Pestka, PhD
Institution: Department of Microbiology, Genetics, & Immunology, Michigan State University
Project Title: Omega-3 Fatty Acids: Omega-3 Effects on Interferon Gene Methylation in Lupus Macrophages
Project Summary: Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by unresolved inflammation and immune complex accumulation, with current treatments often causing significant side effects and being costly. SLE patients exhibit global DNA hypomethylation, particularly in genes related to the type I interferon pathway, which contributes to the persistent interferon signature linked to the disease. This study investigates the potential of docosahexaenoic acid (DHA), an omega-3 fatty acid, as a novel therapeutic approach for SLE. Building on previous findings that DHA suppresses interferon-related gene expression in lupus-prone mice, I hypothesize that DHA induces hypermethylation of SLE-associated genes, thereby reducing disease progression. Using macrophages from lupus-prone Sle123 and wild-type C57BL/6J mice, we will examine the effects of DHA treatment on DNA methylation patterns through methylation sequencing. This research aims to identify epigenetic targets of DHA, elucidate its mechanism of action, and provide preclinical evidence for the potential use of omega-3 fatty acids as therapeutic adjuncts in SLE treatment, offering a promising avenue for developing cost-effective treatments with reduced health risks. Our approach leverages the enhanced genetic tractability of the Sle123 mouse model, which exhibits a lupus phenotype on a C57BL/6J background. The findings from this study could have significant implications for understanding SLE pathogenesis and developing targeted epigenetic therapies, potentially improving the quality of life for SLE patients while reducing treatment-associated complications and high costs.
Rohan Gupta
Mentor: Betty Diamond, MD
Institution: The Feinstein Institutes for Medical Research
Project Title: Determining the Role of the Aryl Hydrocarbon Receptor (AHR) in NPSLE
Project Summary: The aryl hydrocarbon receptor (AHR) is a receptor that has shown promise as a therapeutic target for lupus. For example, a clinical trial is currently investigating the therapeutic effect of tapinarof, an AHR agonist, in treating individuals with cutaneous lupus erythematosus. Research has also shown that treating mice prone to a spontaneous systemic lupus erythematosus (SLE)-like disease benefit from treatment with indole-3-carbinol, a dietary AHR agonist found in cruciferous vegetables. This project will investigate the role of the AHR in neuropsychiatric systemic lupus erythematosus (NPSLE), a type of SLE in which individuals experience neurological and psychiatric symptoms, such as cognitive dysfunction. This project will investigate whether treatment with various AHR agonists, such as indole and indole-3-carbinol, has a therapeutic effect in a mouse model of NPSLE. This project will also investigate whether co-treatment with AHR agonists and captopril (an ACE inhibitor) affects the therapeutic effect of captopril in a mouse model of NPSLE. This is a novel area of research which has the potential to influence clinical treatment of individuals with NPSLE.
Jerik Leung
Mentor: S. Sam Lim, MD, MPH; Cam Escoffery, PhD, MPH, CHES
Institution: Emory University
Project Title: Using Photovoice to Understand Self-Management Behaviors in Lupus
Project Summary: Systemic lupus erythematosus (SLE) and associated comorbidities such as cardiovascular disease and mental health, disproportionately burden Black women. Self-management behavioral mechanisms which underly this disproportionate burden, particularly those that account for the specific sociocultural context of Black women, are underexplored. In this proposal, we describe an examination of the meaning and connected health behaviors of Superwoman Schema (SWS), through centering lived experiences of Black women with SLE in the Atlanta, Georgia metropolitan area. SWS refers to a worldview in which Black women in particular feel compelled to, for instance, be strong for others or put other people’s emotions before their own, when encountering a stressor. SWS may be associated with both behaviors that promote health (e.g., pushing through adversity) and hinder health (e.g., masking pain). Living with a chronic autoimmune disease like SLE presents a specific set of stressors that may influence how SWS manifests in populations of Black women with SLE. Therefore, we propose to use photovoice, a participatory qualitative approach, to understand nuances of SWS among Black women living with SLE. In photovoice, participants are asked to provide photographs and captions in response to a prompt. Participants then convene as a group for a facilitated discussion of the photographs and captions and the discussion, photos, and captions are collaboratively synthesized into themes. We plan to recruit participants through the infrastructure of ongoing Georgians Organized Against Lupus (GOAL) prospective cohort study, based at Emory University School of Medicine. This proposal will advance the knowledge of how to address inequities in SLE by providing a foundation on which to design future disease management interventions.
Sara Smith
Mentor: Gabriela K. Fragiadakis, PhD
Institution: The Regents of University of California, San Francisco
Project Title: Uncovering the Molecular Underpinnings of Lupus Nephritis with Multi-Omic Analysis
Project Summary: Systemic Lupus Erythematosus (SLE), commonly known as lupus, is a complicated autoimmune disease that can affect many parts of the body. One of its most serious complications is lupus nephritis (LN), a condition that damages the kidneys and affects up to 60% of lupus patients. People with LN tend to experience more severe symptoms and worse long-term health outcomes. Scientists know that lupus develops due to a mix of genetic, environmental, and social reasons, but the details of how these elements interact remain unclear.
Current research has identified differences in genetics and chemical markers on DNA that vary between lupus patients. However, these markers are usually studied in isolation, which may overlook important connections between them. In this study, we will use a technique called Multi-Omic Factor Analysis to combine and analyze multiple types of biological data including DNA modifications, single-cell sequencing data (which looks at molecular changes in individual cells), and medical records. Additionally, we will investigate how social and environmental factors may contribute to differences in LN risk among different populations. By uncovering the biological and social drivers of LN, this research aims to pave the way for more precise, personalized treatments that can improve the health and outcomes of lupus patients in the future.
Emma Welter
Mentor: Montserrat Anguera, PhD
Institution: The Trustees of the University of Pennsylvania
Project Title: Investigating the Impact of Lupus-Like Disease on the Inactive X Chromosome in Age-Associated B Cells
Project Summary: Lupus is a debilitating disease caused by overactivity of the immune system, and 90% of patients with lupus are female. The X chromosome contains many genes related to the immune system, and several are implicated in lupus development. Females have two X chromosomes (XX), while males have one X chromosome and one Y chromosome (XY). Thus, it is possible that females express higher levels of immune-related genes from the X chromosome (X-linked genes) compared to males, which could contribute to their heightened susceptibility to lupus. Age-associated B cells (ABCs) are a type of immune cell that is particularly associated with lupus, and inappropriate expression of X-linked genes in females may be linked to ABC development. To prevent expression of genes from both X chromosomes and imbalance of X-linked gene expression between females and males, females undergo X chromosome inactivation (XCI), so that most genes on one of the two X chromosomes are silenced. XCI is regulated by physical association of silencing machinery with the inactive X chromosome (Xi). One component of this machinery is DNA methylation, an epigenetic modification that silences genes. Healthy ABCs and other B cells lack most of the silencing machinery when they are in a resting state and have not yet been activated to respond to an immune challenge. However, resting B cells retain DNA methylation on the Xi, indicating that ABCs might rely on DNA methylation to silence gene expression from the Xi in the absence of other silencing machinery. My proposal will test how gene expression from and DNA methylation on the Xi change with induced lupus-like disease in mice. This will reveal how lupus may upset the balance of gene expression between the two X chromosomes in female ABCs, which may contribute to the female bias seen in lupus patients.
Jin Xuan Zhou
Mentor: Andrea Knight, MD, MSCE
Institution: Hospital for Sick Children, Toronto
Project Title: Diffusion Tensor Imaging Metrics and Neurocognitive Function in cSLE
Project Summary: Childhood-onset systemic lupus erythematosus (cSLE) is an autoimmune disease characterized by inflammation that disrupts neurodevelopment in adolescence. Cognitive dysfunction, including memory, attention, and processing speed difficulties, is common in cSLE patients. These challenges can significantly impact quality of life and result in long-term academic and social consequences. Conventional magnetic resonance imaging frequently detects abnormalities like cerebral hyperintensities and atrophy in SLE, but these findings often fail to correlate with clinical symptoms, limiting their diagnostic utility. Diffusion tensor imaging (DTI), a more sensitive neuroimaging modality, detects subtle microstructural changes in brain tissue that may contribute to cognitive dysfunction in cSLE. Despite its potential, limited research has examined these microstructural changes in cSLE. This study aims to 1) compare brain tissue microstructure between cSLE patients and age-and sex-matched healthy controls using DTI metrics, and 2) explore the relationship between brain tissue microstructure and cognitive processing speed in cSLE patients. Cross-sectional data prospectively collected from 65 cSLE patients and 60 healthy controls aged 10-17 years will be analyzed. Brain tissue microstructure will be assessed using DTI metrics, including fractional anisotropy and mean diffusivity. Cognitive processing speed will be evaluated using the Delis-Kaplan Executive Function System Color-Word Interference Test. Group-level differences in DTI metrics will be assessed using analysis of covariance, and associations between DTI metrics and cognitive processing speed will be examined. This study seeks to provide novel insights into how cSLE affects brain microstructure and neurocognitive outcomes. By leveraging advanced neuroimaging and cognitive assessments, the findings can inform the development of integrated biomarkers for better detecting and monitoring of neuropsychiatric involvement in cSLE.