Research

The team has found that in people with IPF, immune cells in the lungs called macrophages lose their ability to take up iron. These “iron-starved” macrophages appear to promote scarring and are linked to a higher risk of death.

The project asks three questions:

• Can iron levels in the blood or lungs predict how the disease will progress?
• How does a lack of iron uptake make macrophages more harmful?
• Could targeting iron pathways offer new treatments for IPF?

Combining patient samples, advanced imaging and laboratory models, the research aims to help doctors predict outcomes more accurately and to guide new therapies, including repurposing existing drugs that target iron.

Access to patient lung cells is a major obstacle, so the team has developed a model in which patients’ own blood cells are reprogrammed into fibroblasts, the cells responsible for fibrosis.

They have found that a molecule called HE4 is elevated in SSc-ILD and can drive fibrosis, and that a drug already on the market can reduce this fibrosis and inflammation. The project will:

• Characterise the fibrotic and inflammatory effects of the lung microenvironment in SSc-ILD
• Identify licensed drugs that can be repurposed as new antifibrotic and immunomodulatory therapies

The aim is to find drugs that can be used alone or alongside existing therapies to manage SSc-ILD more effectively.

The research focuses on monocytes, cells of the innate immune system. The team has found that monocytes from people with latent TB behave differently from those of healthy people, including in how they use sugar for energy.

The project aims to turn these findings into a new diagnostic tool that uses small blood samples, suitable even for children, tested in infants, children and adults with latent or active TB.

This could lead to a more accurate test to distinguish latent from active TB and to identify those most at risk, helping target treatment and supporting global TB elimination.