2026 Recipients of the Gary S. Gilkeson Career Development Award
Kaien Gu, MD
Mentor(s): Dr. Cynthia Aranow & Dr. Betty Diamond
Institution: The Feinstein Institutes for Medical Research
Project Title: Evaluating T-Dependent & T-Independent Stimulation of B Cells in SLE
Project Summary: Imbalances in certain immune system cells and the production of self-attacking proteins, or autoantibodies, can result in inflammation, leading to some of the symptoms that patients with lupus experience. B cells are an important component in the blood that play a vital role in the production of autoantibodies in patients with lupus. B cells can be further divided into various fractions, and researchers know that the frequency of these subsets are different in individuals with and without lupus. Moreover, while doctors specifically try to target all B cells in some patients with lupus, certain B cell subsets can persist despite our best efforts with currently available treatment.
Think of the B cells like a symphony orchestra – an orchestra requires the perfect balance of string, woodwind, and brass instruments to produce a harmonious sound. But an orchestra would not sound the same if it had too many trombones or too few clarinets. And it would not be the same if there was no conductor or if some of the musicians played out of turn or not at all. Yet while this is what we can see (and hear) happening in some patients with lupus, we do not completely understand how or why this occurs, what mechanisms control B cell development and antibody production, or how this relates to lupus activity and inactivity over time.
Researchers at the Feinstein Institutes for Medical Research in New York aim to further explore B cell proliferation and differentiation further and hope to better understand and answer these important questions. If we know more about how certain B cells develop and differentiate and why autoantibodies arise, we can better discover how lupus occurs, and we might be able to improve symptoms in patients living with lupus by specifically targeting these cells or their precursors
Emma Materne, MD
Mentor(s): Dr. Karen Costenbader
Institution: Brigham and Women's Hospital, Inc.
Project Title: Dissecting SLE Heterogeneity with Metabolomics
Project Summary: Objectives: Systemic lupus erythematosus (SLE) is a complex autoimmune disease that can affect many different parts of the body, including the kidneys, skin, joints and blood. Some people develop severe organ damage, while others have mild disease. Being able to identify organ involvement earlier may help doctors diagnose SLE sooner, choose the most effective treatments, and prevent long-term complications. One promising way to better understand SLE is by studying small molecules in the blood, called metabolites, which reflect how the body uses energy, fats, and proteins. Early research suggests that people with SLE have different metabolic patterns than healthy individuals, and that these patterns may differ depending on which organs are involved. Patients at increased risk for developing lupus may have similar metabolic patterns as patients with SLE. Most previous studies have been small and could not fully account for important factors such as medications, genetics, or disease markers in the immune system.
Methods: We will analyze blood samples, genetic testing and health data from about 400 people with SLE and metabolite levels from blood samples in ~10,600 patients with ANA testing. We will compare metabolic patterns across different forms of SLE, such as kidney disease, arthritis, blood disorders and skin involvement, while also considering other clinical tests and genetic risk. We will then assess metabolite profiles in patients tested for ANA to look for patterns between ANA level and pattern, genetic risk and metabolites levels. Using advanced data analysis methods, we aim to identify metabolic “signatures” linked to specific SLE-related organ disease.
Significance: This work has the potential to improve how SLE is diagnosed and monitored and tailor treatments to the underlying biological processes driving each patient’s disease.