Around 80,000 people in the UK live with multiple sclerosis (MS), a disease where immune cells attack the brain and destroy nerves. Researchers know from mouse models that three types of immune cells—Th1, Th17, and T regulatory (Treg) cells—drive either disease progression or recovery, but they do not understand how these populations interact inside the brain. This project uses new mouse models that allow scientists to track each cell type in real time, revealing whether Th1 and Th17 cells work together or against each other to cause damage, and how Treg cells stop that damage. If successful, the work could lead to therapies that boost Treg activity to halt nerve destruction and promote repair. The team will also search for biomarkers—molecular signals in the blood or tissue—that predict whether a patient’s MS will worsen or improve, enabling doctors to tailor treatments more precisely. This is fundamental science: it does not promise an immediate cure, but understanding the cellular choreography of inflammation is a necessary step toward designing drugs that shift the immune system from attack to repair.
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Around 80,000 people in the UK suffer from multiple sclerosis (MS). Although the precise mechanism that underlie this disease are still poorly understood, there is a consensus that in its early stages there is an ?autoimmune? attack on the brain with immune cells causing inflammation that ultimately destroys the nerves. From a mouse model of MS, called EAE, we know that CD4+ T cells are important both in the development of the disease and in the recovery from disease that can occur. Two types of CD4+ T cells are involved in promoting EAE, so-called Th1 and Th17 cells, and a third type ? T regulatory (Treg) cells are involved in recovery. However, we do not know how these three populations interact during the disease. We have developed new EAE models that allow us to identify and track each cell population within the brain, to determine whether Th1 and Th17 cells work together, independently, or perhaps even against each other to cause the disease. The models will also show how Treg cells can stop the damage caused by Th1 and Th17 cells and will allow us to develop new therapeutic approaches to boost Treg activity. These will also be tested for the ability to promote the repair of damaged nerves. We will also search for new ?biomarkers? which might indicate whether the disease will progress or will recover, and which could be used to better predict the course of MS in patients.
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