Summer 2026 Gina M. Finzi Fellows

The Lupus Foundation of America awarded five individuals to receive the 2026 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 2026 Gina M. Finzi Memorial Student Summer Fellows are:

Alaina Dhawan

Mentor: Dr. Andrea Knight 

Institution: The Hospital for Sick Children, Toronto 

Project Title: Quantitative Susceptibility Mapping of Brain Tissue in cSLE

Project Summary: Childhood-onset systemic lupus erythematosus (cSLE) is an autoimmune disease that can affect the brain. Many young people with cSLE experience difficulties with thinking, memory, mood, or behavior, which can have lasting effects on quality of life. Although magnetic resonance imaging (MRI), a type of brain scan, is often used to look for lupus-related changes, standard MRI findings do not always explain these symptoms and may miss very small or early changes in brain tissue.

This study will use a newer and advanced brain imaging method called quantitative susceptibility mapping (QSM). QSM is a specialized type of MRI that can detect subtle changes in brain tissue related to iron levels and microscopic structure. These changes may reflect inflammation or injury that is not visible on routine brain scans.

The goals of this study are to compare brain tissue measurements from QSM scans between adolescents with cSLE and healthy adolescents of the same age and sex. The study will also explore how these brain changes relate to lupus features such as disease duration, disease activity, medication use, and overall disease impact. The study will analyze existing brain MRI data from patients followed at The Hospital for Sick Children.

By combining advanced brain imaging with clinical information, this research aims to improve understanding of how lupus can affect the developing brain. These findings may help identify new imaging markers that could support earlier detection, better monitoring, and improved care for children and adolescents living with lupus. 

Delaney Ding

Mentor: Dr. Renee Modica 

Institution: University of Florida 

Project Title: Cutaneous Disease Burden and Trajectories in Childhood-Onset Lupus 

Project Summary: Skin problems such as rashes, hair loss, and sores are common in children with lupus, but they are often overlooked or dismissed. Many patients and families report that skin disease has a major impact on daily life, self-esteem, and overall well-being, yet it is not consistently measured or followed over time.

This project will use information already collected in a large international pediatric lupus registry to better understand how skin disease affects children with lupus. We will identify which children experience skin involvement, how these skin symptoms change over time, and how they relate to other aspects of lupus such as disease activity, treatment patterns, and how patients feel about their health overall.

By focusing on patient-reported health and longitudinal clinical data, this study aims to show that lupus skin disease is more than a cosmetic issue and plays an important role in the overall burden of disease. The results may help clinicians better recognize, monitor, and address skin involvement in children with lupus, and support future research that centers on outcomes most important to patients and families. 

"Mansoor" Mohammad Mansoor

Mentor: Dr. Wen-Yuan “Elena” Hsieh & Dr. Mia Smith

Institution: University of Colorado Denver, AMC and DC

Project Title: Characterizing Polyreactive B-T Cell Dysregulation in Pediatric Lupus

Project Summary: Systemic lupus erythematosus (SLE) is an autoimmune disease in which the immune system mistakenly attacks the body’s own tissues. When lupus begins in childhood (under the age of 18), it is often more severe and requires stronger treatments, yet the pathogenesis of pediatric lupus remain poorly understood.

The immune system normally removes harmful immune cells before they can cause damage. However, a small group of immune cells is allowed to remain because they help protect against viral infections. These cells are known to respond broadly to many targets and are important for fighting viruses such as Epstein-Barr virus and flu. In lupus patients, this group of cells is unusually expanded, raising the possibility that they may also contribute to disease.

This project tests the idea that viral infections trigger these normally helpful immune cells and cause them to become harmful in pediatric lupus. We will study blood samples from pediatric lupus patients to assess if the cells making disease-causing antibodies are also the cells that respond to viruses. Further, we will assess if other immune cells help in this process. By identifying how viral infections may initiate autoimmune responses in children, this work aims to uncover early disease mechanisms and lay the groundwork for future targeted therapies that could prevent or treat pSLE more safely and effectively. 

Gillian McClennen

Mentor: Daniel Fernando Zegarra Ruiz

Institution: University of Virginia School of Medicine

Project Title: Loss and Restoration of Functional Microbial Pathways in Lupus

Project Summary: Systemic Lupus Erythematosus (SLE) is an autoimmune disorder affecting over five million people globally. This chronic condition can cause joint pain, fatigue, cognitive difficulties, and a facial "butterfly rash”. SLE is a complex disease influenced by factors including genetics, environment, and gender, and there are currently no effective treatments that target its underlying causes. Instead, most therapies rely on suppressing the immune system, which can lead to drug-related toxicity and increased vulnerability to infection. The gut microbiome, the community of microbes in our gut, plays a key role in shaping the immune system and autoimmune diseases such as lupus. Lupus is associated with changes both in which microbes are present in the gut and, importantly, in how the gut microbiome functions. For example, the ability of the gut microbiome to produce beneficial nutrients from dietary fiber may be reduced in lupus patients and in mouse models of lupus. Studies in mice suggest that these functional changes can occur even before lupus symptoms develop.

In this study, I will compare gut microbiome functional changes in lupus-prone mice with changes observed in SLE patients to identify shared patterns that are relevant to human disease. To do this, I will use an established computational pipeline to analyze functional changes in open-access gut microbiome datasets from SLE patients and compare these results to changes already identified in mouse studies. One such change observed in mice is a reduced ability of the microbiome to produce butyrate, an anti-inflammatory nutrient, even before lupus symptoms appear. In this study, I will test the impact of this change by treating mice with or without butyrate at different ages and assessing lupus-related symptoms. These studies will investigate which functional microbiome changes observed in mouse studies are present in the SLE patient microbiome and how correcting these changes can alleviate lupus severity. 

Yuri Singh

Mentor: Eduardo Gomez-Banuelos

Institution: Johns Hopkins University School of Medicine

Project Title: The role of autoantibodies against DNA: RNA hybrids in SLE pathogenesis

Project Summary: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by autoantibodies directed against multiple antigens. A predominant and pathogenic subset of autoantibodies targets double-stranded DNA (dsDNA). Current models attribute the autoimmune response against nucleic acids in SLE to defective clearance of extracellular dsDNA due to impaired DNase activity; however, canonical B-form of DNA is relatively not immunogenic, leaving the initiating antigens driving immune responses to dsDNA undefined. We hypothesized that DNA: RNA hybrids or R-loop, a structural variant of DNA, formed during gene transcription and DNA damage, could have greater immunogenic potential than canonical dsDNA. In particular, since DNA: RNA can elicit more robust interferon responses via CGAS, and Toll-like receptor pathways, than canonical DNA. Consistent with this hypothesis, our preliminary experiments showed that patient-derived monoclonal dsDNA antibodies bind DNA: RNA hybrids with greater affinity, confirming the presence of human antibodies that recognize DNA:RNA hybrids, and suggesting that antigen-selection of anti-dsDNA may occur against hybrids. Building on these observations, we will determine the prevalence of antibodies targeting DNA:RNA hybrids in a prospective cohort of SLE, and define their associations with clinical phenotypes, disease activity and molecular endotypes. If successful, these studies will establish DNA:RNA hybrids as autoimmune epitopes in SLE and would provide a mechanistic link between nucleic acid structure and immunogenicity, enable development of novel biomarkers, and reveal new therapeutic avenues to modulate pathogenic nucleic acid sensing in lupus.