Rod Rahimi, MD, PhD

Despite advances in care, many people living with asthma suffer from persistent symptoms and life-threatening exacerbations. Allergic asthma is the most common asthma type and is driven by an abnormal immune response against inhaled allergens. The immune cells implicated in this process are called T cells. In contrast to disease-causing T cells, regulatory T cells (Tregs) are specialized cells that play an important role in inhibiting inflammation. We want to understand how to improve the ability of Tregs to suppress disease-causing T cells in asthma. Using a model of allergic asthma, we have found a unique population of immune cells within the airways, called dendritic cells, which produce attractive signals for Tregs. We have developed new experimental models to study how dendritic cells recruit Tregs to suppress disease-causing T cells in allergic asthma. Our goal is to develop new treatments to improve the lives of individuals with allergic asthma.

Update:

Using a mouse model of allergic asthma, we have found a unique population of cells called cDC2s that produce attractive signals for Tregs during allergic inflammation. We have generated novel experimental tools to test the role of these Treg-attracting cDC2s in allergic airway inflammation. We have found that uniquely impairing the ability of Tregs to be attracted by cDC2s during allergic inflammation led to a dramatic increase in the number of disease-causing T cells in the lungs and a worsening of the airway disease. We are defining the precise mechanisms whereby cDC2s promote the ability of Tregs to suppress disease-causing T cells and allergic inflammation. By understanding how Tregs suppress, and fail to efficiently suppress, allergic inflammation, we hope to identify new treatment approaches to enhance the ability of Tregs to suppress allergic asthma.