David Greaves read Microbiology at Bristol and studied for a PhD in Biophysics and Molecular Biology at King’s College London (Winner of the Tadion-Rideal Medal). Postdoctoral research was undertaken at the Netherlands Cancer Institute in Amsterdam, the National Institute for Medical Research at Mill Hill in London and the Sir William Dunn School of Pathology in Oxford before being awarded a British Heart Foundation Basic Science Lectureship and subsequent election to a University Lectureship in Cell Pathology. In 2010 David Greaves was awarded the title of Professor of Inflammation Biology by the University of Oxford.
David Greaves leads the Hertford Medicine teaching team. Prof. Greaves tutors first year students for Biochemistry & Medical Genetics, Endocrinology and Cell Biology. He also tutors second year BM Principles of Pathology and third year modules in Cardiovascular Pathology and Innate Immunity.
Prof. Greaves is the Course Director of the Oxford 4-year Cardiovascular Sciences DPhil course, which awards four 4-year British Heart Foundation studentships a year. Prof. Greaves currently supervises three DPhil students in his laboratory.
Inflammation Biology – Acute Inflammation is the response of all tissues to injury and infection. Inflammation is characterised by the rapid recruitment of plasma proteins and white blood cells called neutrophils from the bloodstream. This process is usually short lived and is followed by a period of inflammation resolution when dead microbes, cell debris and dying host cells are removed by cells called macrophages.
Chronic inflammation is characterised by continuing inflammation and the build up of large numbers of macrophages and lymphocytes in diseased tissues such as the joints in rheumatoid arthritis. Work in the Greaves laboratory is aimed at understanding the key molecules that recruit and retain macrophages at sites of chronic inflammation and understanding the key pathways that initiate inflammation resolution.
Cardiovascular disease – Angina, heart attacks and ischaemic strokes are all caused by the same underlying disease process in arteries called atherosclerosis. Atherosclerosis is characterised by the build up of cholesterol containing lipoproteins and macrophages within the lining of major arteries.
Professor Greaves and collaborators within the Department of Cardiovascular Medicine are studying the molecular mechanisms that regulate the very earliest stages of atherosclerosis and investigating factors within atherosclerotic plaques that affect macrophage differentiation.
In collaboration with Professor Ed Fisher at New York University we are examining models of atherosclerotic plaque regression with a special emphasis on how macrophage responses to chemokines can be modified by diabetes and hypertension.
Anti-inflammatory drug development – Recent work from the Greaves laboratory has shown that an FDA approved medicine called ibrutinib used for the treatment of a rare form of cancer has potent anti-diabetic and anti-inflammation effects that work by altering macrophage cell signalling. In current experiments we are exploring if this drug can have beneficial effects on macrophage cell biology in atherosclerosis.
Selected recent papers from over 150 peer-reviewed articles: