Research Award 2025 (1)

Dr Thomas Bond, Clinical Research Fellow in the Department of Medicine, University of Cambridge

Research Project: Analysing the effects of anifrolumab on arterial inflammation in patients with active SLE

Autoimmune conditions can cause both short and long term damage to the blood vessels and heart (the cardiovascular system). Cardiovascular involvement in autoimmune conditions often goes undetected until a late stage in the disease when preventative treatments may be less effective.

As a result, people with autoimmune conditions have an increased risk of cardiovascular disease. Patients with the autoimmune condition Systemic Lupus Erythematosus (SLE) have double the risk of disease in their arteries and heart tissue which can lead to heart attacks, stroke and heart failure. The risk of heart attacks in female patients with SLE aged 35 to 44 years old is 50 times higher than women of the same age who do not have SLE.  Although the excess cardiovascular risk in SLE is known to be caused by inflammation, whether therapies given for SLE can also lower cardiovascular inflammation is unknown.

In this study, a specialised imaging test called positron emission tomography (“PET”) will be used to measure inflammation in the blood vessels and heart in patients who require treatments for SLE as part of their clinical care. A PET scan involves injecting a “tracer” to detect biological processes such as inflammation by labelling cells with a small amount of radioactivity that is localised by the PET scanner. Our research has shown that a PET tracer called “68Ga-DOTATATE” can identify inflammation in the cardiovascular system by labelling immune cells known as macrophages.

In this project, we will use PET imaging with 68Ga-DOTATATE, as well as computed tomography (CT) and magnetic resonance imaging (MRI), to observe changes in cardiovascular inflammation after treatment with therapies for SLE. Our study will examine the SLE therapy anifrolumab that blocks the action of an inflammation-causing molecule called interferon. This treatment is known to improve clinical markers of SLE disease activity, but we will assess their effects on inflammation in the blood vessels and heart.

As well as imaging inflammation, we will examine whether SLE treatments affect the ability of blood vessels to dilate in response to a drug infusion. This test provides a marker of vascular health associated with cardiovascular risk. We will also measure immune cells and proteins in the blood, before and after treatment, to better understand how SLE drugs affect levels of inflammation in the body that cause cardiovascular disease.

This research will provide new knowledge about the link between autoimmune conditions and cardiovascular disease, and whether targeting the immune system with therapies used in SLE could reduce levels of inflammation in the cardiovascular system.  This work will advance approaches towards managing CVD in people with IMIDs, with potential wider implications for drug re-purposing to treat CVD in the general population.

 

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