My research programme seeks to make fundamental discoveries about the immune system, centred on the immune response to the malaria parasite Plasmodium falciparum. We do this for two main reasons. First, by understanding the immune response to Plasmodium parasites better, we can help develop better vaccines for malaria. Second, complex parasites like malaria, which deploy multiple strategies to evade the immune system, can teach us about aspects of immune function that are not visible when studying simpler pathogens or immunisations.

We study a wide range of aspects of immunology, from the innate to the many arms of the adaptive immune response. We have recently shown how parasites are detected by the immune system via their ability to traverse and consequently injure cells en route to the liver, the site of infection (Nature Microbiology, 2026). However, the main focus of the lab has been on understanding B cell responses to parasites. We have shown how the high antibody titres required for protection can limit the immune response via a negative feedback process (Cell Host & Microbe, 2020). This matters because it means targeting a single vaccine antigen alone will not be sufficient to confer protection. To overcome this, we have developed animal models that ignore the main vaccine targets for malaria, revealing other protective responses that we can now target with new vaccines (Science Immunology, 2025).

We are also interested in the molecular control of these immune responses, as ultimately the molecules controlling the immune system are potential drug targets. We identified the transcription factor Zeb2 as key to the control of a population of B cells called atypical B cells (Science Immunology 2024). These cells are most commonly seen in chronic infection (where they may be beneficial) but also in autoimmunity (where they can cause disease). Most recently, we begun to explore how epigenetic marks can control cell fate decisions and support the maintenance of immune cells.