About
Miguel Fribourg, PhD
I am an Assistant Professor at the Icahn School of Medicine at Mount Sinai in the Institute for Translational Medicine and Pharmacology and the Department of Pharmacological Sciences. My research integrates engineering, computation, and immunology to understand immune signaling, immune regulation, and immune-mediated disease. I lead the Fribourg Lab, where we develop quantitative and experimental approaches to study immune cell behavior and inform translational immunology.
My scientific training spans engineering, signal processing, biomedical sciences, and experimental immunology, shaping a systems-level approach to biological questions. This multidisciplinary background enables me to integrate high-dimensional experimental data with mechanistic and computational analysis, bridging molecular mechanisms with complex immune phenotypes relevant to human disease and therapeutic intervention.
My long-term goal is to establish generalizable computational frameworks for immune regulation that connect fundamental immunology with translational pharmacology and clinical decision-making across immune-mediated diseases.
Contact Information
Icahn School of Medicine at Mount Sinai
Atran Berg Laboratory Building
Floor 4 Room Room AB4-45
1428 Madison Ave
New York, NY 10029
miguel.fribourg@mssm.edu
Appointments & Positions
Assistant Professor, Institute for Translational Medicine and Pharmacology, Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai (2026–present)
Assistant Professor, Translational Transplant Research Center, Department of Medicine, Icahn School of Medicine at Mount Sinai (2018–2025)
Research Assistant Professor, Department of Neurology,
Icahn School of Medicine at Mount Sinai (2016–2018)
Education & Training
Ph.D., Signal Processing — Universidad Politécnica de Madrid, Spain
Postdoctoral Training, Systems Biology and Immunology — Icahn School of Medicine at Mount Sinai, USA
Ph.D., Biomedical Sciences — Icahn School of Medicine at Mount Sinai, USA
B.Sc., Chemistry — Universidad Nacional de Educación a Distancia (UNED), Spain
M.Sc., Telecommunication Engineering — Norwegian University of Science and Technology, Norway
B.Sc., Telecommunication Engineering — Universidad Politécnica de Madrid, Spain
Selected Contributions to Science
My contributions to science span quantitative modeling, immune signaling, and translational immunology, with an emphasis on uncovering mechanistic principles through the integration of computation and experimentation
1. GPCR heterocomplexes and antipsychotic drugs
Elucidated the mechanism of action of antipsychotic drugs through GPCR heterocomplexes involved in schizophrenia. By studying the heteromer formed by the Gi-coupled metabotropic glutamate receptor 2 (mGluR2) and the Gq-coupled serotonin receptor 2A (2AR), this work provided an integrated theory explaining psychosis and hallucinations and how antipsychotic drugs modulate serotonin/glutamate signaling.
2. Immune genomics data integration
Created data-integration resources to enable systems-level analysis of immune genomics. This work distilled 38,088 genome-scale experiments into immunological networks of functional relationships between molecular entities (ImmuNet), with publicly accessible tools for data mining and hypothesis generation.
3. Computational models of immune responses
Developed computational models and quantitative techniques to study innate and adaptive immune responses. These include stochastic models of viral infection and type I interferon signaling, ordinary differential equation models of alloimmune responses, and biosensor- and FRET-based approaches to measure T cell function.
4. Interferon-β mechanism in MS and transplantation
Uncovered the mechanism of action of interferon-β in immune regulation and transplantation. Using experimental transplant models, in silico analysis, and human immune cell studies, this work demonstrated that IFN-β directly promotes regulatory T cell induction via STAT1- and p300-dependent Foxp3 acetylation, identifying an unexpected mechanistic link with therapeutic implications for transplantation, autoimmunity, and malignancy.
5. Immune signatures in transplant recipients
Identified transcriptomic and phenotypic immune signatures associated with improved transplant outcomes. This includes peripheral blood transcriptomic signatures linked to successful calcineurin inhibitor withdrawal, phenotypic markers of T cell exhaustion associated with improved graft function, and spatial transcriptomic pipelines applied to kidney transplant biopsies to define gene expression patterns associated with acute T cell-mediated rejection.
