Assistant Professor, Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania Dr. Joel Babdor is an Assistant Professor of Systems Pharmacology and Translational Therapeutics at […]
Applying self-supervised AI to multi-modal electronic health records — integrating clinical notes, labs, and imaging — this project builds scalable diagnostic models to detect autoimmune diseases earlier and more precisely.
Identifying a novel molecular regulator of tolerogenic dendritic cell function, this project uncovers how its loss triggers spontaneous multiorgan autoimmunity and exacerbates lupus — revealing a clinically relevant pathway in immune tolerance.
A self-replicating RNA platform delivers anti-inflammatory cytokines directly to the airways, offering targeted local immune suppression without systemic toxicity — a mechanistically distinct approach to treating lupus lung disease.
By profiling genetic and molecular drivers of pemphigus vulgaris across patient skin and blood, this project uncovers genotype-driven inflammatory loops and actionable targets for personalized therapy.
Integrating clinical, imaging, and biological data from large real-world MS cohorts, this project builds a machine learning model to predict disability progression early and enable personalized treatment decisions.
Investigating how foreign sugar modifications on anti-TNF biologics trigger immune responses in pediatric IBD patients, this project aims to personalize biologic therapy selection and inform safer drug design.
Combining machine learning with microbiome and metabolomic data from 4,000+ IBD patients, this project develops tools to predict disease flares, identify therapeutic targets, and enable personalized flare prevention.
Applying advanced quantitative MRI to detect pathology invisible to current clinical tools, this project builds an AI model to predict MS progression and enable earlier, more personalized diagnosis and treatment.
Developing novel multivalent small molecules that selectively silence or eliminate the autoantibody-producing B cells driving autoimmune disease.
