IgE-mediated allergic diseases such as asthma are increasing in westernized countries; however, the mechanisms leading to development of these diseases are unknown. The overall goal of Dr. Mitchell Grayson’s research is to understand the immunological mechanism(s) that lead to the development of these diseases, focusing specifically on translation of the antiviral immune response into allergic disease and asthma. Using the Sendai virus (murine parainfluenza virus) model, his group characterized the role conventional and plasmacytoid dendritic cells play in the antiviral immune response. They were the first to demonstrate that production of Sendai virus–specific IgE and lung dendritic cell expression of high-affinity IgE receptor (FcεRI) during the antiviral immune response is critical for the translation of the viral infection into allergic disease. His group then identified a novel neutrophil subset that was required to induce lung dendritic cell expression of FcεRI during the antiviral immune response. Further, they have shown that exposure to a nonviral antigen during the viral infection is sufficient to drive an allergic response against the nonviral antigen. Together, these data provide a mechanistic explanation suggesting that respiratory viral infections underlie the development of allergic diseases and asthma. His group has also shown that these immunological mechanisms are present in humans.
Mitchell Harry Grayson, MD