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Dendritic cells play important roles in inducing immunity against microbial antigens while developing tolerance against self or innocuous foreign antigens. Our laboratory is interested in identifying the specific mechanism by which dendritic cells mediate regulatory T cell (Treg) development and defining the biological impact that dendritic cells make on immune suppressive function of Treg. Our recent study implicates the role of Membrane-Associated RING finger CH 1 (MARCH1) ubiquitin ligase in dendritic cell selection of natural Treg. Current research focuses on defining the molecular mechanism by which MARCH1 mediates Treg development and determining functional specialization of Treg generated in this MARCH1-dependent manner.

Our laboratory is also interested in understanding how dendritic cells participate in IgE-mediated asthma pathogenesis. Asthma represents a serious inflammatory airway disease affecting hundred millions of adults and children in the world. IgE is one of the most important pathologic players in this disease, however the underlying mechanism is not completely understood. Our recent study indicates that dendritic cells constitutively internalize circulating IgE via the high affinity IgE receptor (FceRI) and promote serum IgE clearance, which implicates dendritic cells in IgE turnover. In asthma however, dendritic cells accumulate IgE at their surface and infiltrate airway epithelium, suggesting functional alteration and contribution of dendritic cells to this disease. Current research aims to identify the molecular mechanism by which FceRI mediates internalization of IgE in dendritic cells and determine the specific contribution that these cells make to asthma.