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Research & Initiatives


How does the immune response remember what it has encountered?

The basis for much of the work going on in the lab revolves around two major cells of the immune system: T cells and B cells. T cells are immune cells that can either “help” other immune cells perform their job better or directly kill cells that are infected with a virus. B cells are the antibody factories of the immune system and provide antibodies to combat a wide range of infectious pathogens. One of the hallmarks of these immune cells is that they can “remember” previous pathogens (or vaccines) that they have encountered. This immune memory is responsible for why vaccines are effective or why when you are infected with a bacteria or virus a second time, you don’t get sick. Using both infection models and vaccination models, we seek to understand how different types of “memory” are created in these immune cells so that we can design better vaccines of other therapies that can generate the best and most powerful immunity to a wide range of pathogens.

Can vaccines be manipulated to redirect optimal immune responses to where they are most needed?

Most pathogens enter the body at surfaces that interact with the outside world, such as the lungs, intestines, and female reproductive tract. For pathogens such as this, it is desirable to direct vaccine-induced immune cells to their initial entry point, called mucosal tissues, but it is unclear how this might happen or whether this is possible using traditional vaccines. While it is known that vaccines given via traditional routes, i.e. intramuscularly, can protect against many infectious diseases, it is less clear how changing routes or vaccine make-up can affect immune cell migration or protection. Does immunizing in skin direct a different response compared to immunizing via another route? Does the type of adjuvant (substance added to a vaccine to boost the immune response) change the predominant immunity from antibody-dominated to one that is more cell-mediated? We are investigating these questions using a variety of sophisticated immunological tools. Our goal is to be able to imprint an anatomical “zip code” for the correct type of cells against a particular pathogen based purely on vaccine design.


Why do men and women differ immunologically and how can this be exploited to develop better vaccines?

One of the great questions in biology is why men and women differ in how they respond immunologically to various insults. It is known that women respond better to vaccines and many infections, yet this increased immune response often manifests in increased susceptibility to autoimmune disease in women compared to men. In fact, women are three times more likely to be diagnosed with multiple sclerosis and nine times more likely to have lupus when compared to men of a similar age. We are interested in understanding the mechanisms that dictate these differences. Using mouse models, we are exploring how males and females respond to infection, vaccination, and autoimmune disease induction. We are particularly interested in defining how T cell and B cells might behave differently in different tissues and whether the differences we see are cell intrinsic (programmed into the cell when it develops) or cell extrinsic (changes depending on the surrounding environment). Revealing how these disparities are established could lead to potential therapies for autoimmune diseases or help in designing more effective vaccines depending on the sex of the person receiving the immunization. 

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