SUMMIT 2023: Meet the Speakers!

Lisa Wagar, PhD

Assistant Professor in the Department of Physiology & Biophysics at the University of California Irvine

Lisa Wagar is an Assistant Professor in the Department of Physiology & Biophysics at the University of California Irvine. Dr. Wagar earned her PhD from the University of Toronto and completed a postdoctoral fellowship at Stanford University in Dr. Mark Davis’s lab. The foundation of her lab’s research is investigating how the specialized microenvironment of lymphoid tissues regulates antigen-specific adaptive immune responses. Dr. Wagar’s group uses an immune organoid model derived from primary human lymphoid tissues to study how a variety of host factors and antigen factors contribute to inter-individual differences in vaccine responses.

Talk: TBA

Abstract:  The essential features of a highly effective vaccine are that it stimulates a robust, specific, and durable adaptive immune response. For respiratory pathogens, an effective vaccine should also elicit a local immune response in the respiratory tract to mediate protection. Historically, vaccine testing has been largely empirical, so it has been challenging to rationally design vaccine candidates with these properties. Additionally, responses in animal models are poorly predictive of vaccine responses in humans. To bridge the current gap in informed vaccine design, it is therefore critical that we understand the cellular dynamics underlying human adaptive immune responses during a vaccine response. To achieve this, we use a human immune organoid model derived from primary tonsil tissues that are collected from otherwise healthy tonsillectomy patients. In our recent work, we used the tonsil organoid model to track antigen-specific B and T cell responses to influenza antigens using a multi-omics approach, including high parameter flow cytometry. Each antigen format elicited distinct B and T cell responses, including differences in their magnitude, diversity, phenotype, function, and breadth. These differences culminated in striking changes in the corresponding antibody response. We show that a major source of antigen-associated variability lies in the recruitment of naive vs. memory B cells to the response. These findings have important implications for vaccine design and the generation of protective immune responses against respiratory pathogens.