Our model on how inflammatory responses to blood-stage Plasmodium parasites inhibit the differentiation of a population named T follicular helper cells that are pivotal in the induction of antibody responses to infection.
When a person is exposed to a pathogen, the immune system attempts to mount a defence against it. When the defence is successful, immunity results. In the process of developing immunity, the body produces substances known as antibodies against a specific germ and creates a “memory” of this experience that can be called upon for protection, when needed many months or years later. The next time the person encounters that pathogen, the antibodies that circulate in the bloodstream prevent it from causing disease and eliminate the germ from the body.
Unlike other infections in which one single encounter with the pathogen is enough to induce long-lasting protection, immunity to malaria might take decades to develop in endemic areas. The Hansen Lab investigates mechanisms by which Plasmodium infections prevent the acquisition of immunity. This work is undertaken in order to design therapeutic approaches to improve the induction immune responses to the Plasmodium parasite, including effective anti-malaria vaccines.
Clinical immunity to malaria is largely dependent on effective antibody responses. In collaboration with partners in malaria-endemic countries, our group investigates how the induction of antibody-mediated immunity is dysregulated during symptomatic malaria and how constant exposure to Plasmodium parasites over time modulates the development of these responses.