UT Southwestern Allergic Disease and Antiviral Responses Program

The collective goals of the Allergic Disease and Antiviral Response Program seek to understand the cellular and molecular interactions between allergic stimuli and viral infections. These studies are based on the premise that upper respiratory viral infections 1) contribute to the etiology of allergic asthma, 2) are associated with allergic asthma and rhinitis exacerbations, and 3) are a primary factor driving allergic morbidity and mortality. Central to these studies is the primary anti-viral cytokine, type I interferon (IFN-α/β). Over the last 6 years, Drs. Farrar and Gill discovered an important reciprocal negative regulatory pathway, which involves both the expression and biological activity of IFN-α/β in the context of allergic diseases. Dr. Farrar’s group discovered that IFN-α/β potently inhibits both the development and stability of Th2 cells, which are the main mediators of allergic inflammation and the drivers of IgE class switching in B cells. In parallel, Dr. Gill’s team found that FcεR signaling via IgE crosslinking on dendritic cells blocked the secretion of IFN-α/β in response to viral infection. To learn more about these studies, click the links within the diagram above.