We investigate how redox biology, T cell metabolism, beta cell stress, antigen recognition, and early immune biomarkers shape the development of type 1 diabetes. Our research combines mechanistic immunology with translational models to identify earlier signals of disease and new opportunities for therapeutic intervention.
Select a production to jump directly to publications connected with that research theme.
We study how reactive oxygen species and redox-sensitive signaling shape innate and adaptive immune activation in type 1 diabetes.
This work examines how redox cues influence inflammatory signaling, T cell activation, immune tolerance, and beta cell vulnerability.
View related publications →We investigate how nutrient use and metabolic reprogramming support autoreactive T cell activation, persistence, and effector function.
By targeting glycolysis and related metabolic pathways, we aim to identify mechanisms that can selectively restrain pathogenic T cell responses.
View related publications →We examine how endoplasmic reticulum stress, oxidative stress, autophagy defects, and inflammatory signals alter beta cell function and immune visibility.
A major focus is how stressed beta cells generate or expose altered antigens that can intensify autoimmune recognition.
View related publications →We develop biomarkers designed to detect immune activation before overt type 1 diabetes and to better define dynamic windows of disease progression.
Current work includes soluble LAG-3 as an early readout of T cell activation in self-reactivity, at-risk populations, and broader immune responses.
View related publications →We track autoreactive T cell populations to understand activation, antigen recognition, diversification, and tissue-specific enrichment during autoimmune progression.
These studies use diabetogenic T cell models, peptide–MHC tetramers, and longitudinal sampling to connect antigen specificity with disease biology.
View related publications →We use preclinical systems and human samples to test mechanisms discovered in the lab and evaluate strategies that protect beta cells or redirect pathogenic immunity.
This includes adoptive-transfer models, therapeutic perturbations, islet biology, and translational studies designed to bridge mechanism with clinical relevance.
View related publications →
Spontaneous and induced autoimmune diabetes models allow us to follow immune activation, beta cell injury, disease progression, and therapeutic response in vivo.
Defined diabetogenic T cell populations are transferred into recipient mice to study the timing, phenotype, antigen reactivity, and tissue localization of autoimmune responses.
Multiparameter flow cytometry defines immune populations, activation states, checkpoint expression, regulatory phenotypes, and tissue-specific changes at single-cell resolution.
Peptide–MHC tetramers identify antigen-reactive T cells and allow us to track specificity, co-reactivity, expansion, and diversification over time and across tissues.
Redox-sensitive pathways are manipulated and measured to determine how reactive oxygen species influence immune activation, inflammatory signaling, and beta cell health.
Metabolic assays define how glycolysis, mitochondrial activity, nutrient availability, and metabolic checkpoint pathways sustain autoreactive T cell function.
Histology, molecular assays, and tissue-level analyses connect beta cell stress, islet inflammation, antigen presentation, survival, and immune infiltration.
ELISA, RNA-based measurements, and related molecular assays quantify soluble immune markers, beta cell stress signals, and longitudinal changes associated with disease.
Human plasma and longitudinal samples connect mechanistic discoveries to first-degree relatives, autoantibody status, disease progression, and clinically relevant immune states.
Candidate interventions are tested in mechanistic and disease models to determine whether they can redirect pathogenic immunity, preserve beta cell function, or improve outcomes.