My research focuses on asthma, specifically on understanding the mechanisms driving disease severity. Severe asthma is defined as asthma requiring treatment with high dose inhaled corticosteroids plus a second controller and/or systemic corticosteroids to prevent it from becoming "uncontrolled" or asthma that remains "uncontrolled" despite this therapy. Severe uncontrolled asthmatic patients represent a distinct endotype with persistent airway inflammation and remodeling refractory to corticosteroid treatment, with changes in airway structural cells leading to progressive worsening of airflow obstruction and reduced breathing capacity. CD4+ T cells and their canonical effector molecules, like type 2 cytokines, play a central role in orchestrating asthma pathogenesis, and therapies targeting these cytokine pathways have had promising outcomes. However, only up to 50% of patients respond to treatment, and their effects are neither durable nor reverse airway remodeling in all cases. My goal is to elucidate how a specific CD4+ tissue-resident memory (TRM) T cell subset identified through single-cell RNA-sequencing in the airways of these severe asthmatic patients may be the driver of airway inflammation and how its interaction with airway structural cells may drive remodeling events in severe asthma.

I study immune regulation by regulatory T cells in intestinal inflammation.