Background

Over the past 14 years, I have gained multi-disciplinary training in cancer immunology, autoimmunity, immune aging, early life immunity, and computational biology. My current research employs systems immunology approaches to investigate immune remodeling across the human lifespan.

The Jackson Laboratory for Genomic Medicine | Farmington, CT, USA

Research Scientist | 2023 - now (Ucar lab)
Associate Research Scientist | 2019 - 2023 (Banchereau lab, then Verhaak lab)
Postdoctoral associate | 2016 - 2019 (Banchereau lab)

Throughout my career at the Jackson lab, I have successfully led collaborative studies and developed computational frameworks to analyze genomic datasets, including single-cell (scRNA-seq), ATAC-seq, and spatial transcriptomics. My primary projects include:
1) Pediatric SLE patient classification through single-cell derived genomic signatures. I developed computational pipelines using bulk and scRNA-seq to analyze large-scale datasets and enhance the accuracy of SLE patient classification.
2) NK-like senescent CD8+ T cells that expand with age. I built computational frameworks to profile age-related immune senescence.
3) Longitudinal evaluation of the immune response to the first set of routine vaccines in infants. I contributed significantly to the creation of computational models for studying immune cell dynamics in two-month-old infants.
4) Characterization of the immune perturbations in two-month-old infants with severe COVID-19. I leveraged scRNA-seq, cytokine profiling, and antibody analysis to develop and automated a multi-omic computational framework for studying COVID-19 in infants and compare their immune responses to those of infected children and adults.

Early research: Sorbonne University | Paris, France

During my predoctoral training (Klatzmann lab; University Pierre & Marie Curie, Paris, France; 2010-2016), I focused on understanding why embryos and tumors expressing foreign antigens were not rejected by the immune system. Using murine models (pregnant mice and mice injected with different tumor models), I demonstrated that a specific CD4+ T cell population, the regulatory T cells (Tregs), orchestrates similar immune evasion mechanisms in both fetuses and tumors. Using both transcriptomic profiling and flow cytometry analysis of the tumor microenvironment, we demonstrated that co-silencing of TGF-β and VEGF led to a substantial spontaneous tumor eradication rate and the combination of their respective inhibitory drugs was synergistic. A collaboration with the Aryee lab (Massachusetts General Hospital & Harvard Medical School) allowed us to confirm our findings on the similarities between tumor and fetal development in humans.