Professor David Greaves
Tutorial Fellow in Medicine
Professor of Inflammation Biology
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. In 2002 David was elected to a University Lectureship in Cell Pathology and in 2010 he was awarded the title of Professor of Inflammation Biology by the University of Oxford.
Find out more on his Faculty profile.
Undergraduate teaching
Professor Greaves leads the Hertford Medicine teaching team. He tutors first-year students in Biochemistry, Medical Genetics, and Cell Biology. He also tutors second-year BM Principles of Pathology and third-year modules in Cardiovascular Pathology and Innate Immunity.
Graduate teaching
Professor Greaves has been a Course Director of the Oxford four-year Cardiovascular Sciences DPhil programme since 2005. This scheme awards British Heart Foundation (BHF) studentships for graduate students to work on all aspects of cardiovascular disease. Details of the new BHF Cardiovascular Rewind graduate student scheme can be found here.
He currently supervises three DPhil students in his own laboratory and is college advisor for ~20 graduate students at Hertford College.
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Research interests
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 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 pathways that initiate the process of inflammation resolution.
Cardiovascular disease – Angina, heart attacks and ischaemic strokes are all caused by a disease process in arteries called atherosclerosis. Atherosclerosis is characterised by the deposition of cholesterol containing lipoproteins and an accumulation of 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 studying macrophage gene expression in atherosclerosis.
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-inflammatory effects that work by altering macrophage cell signalling.
Macrophage chemotaxis and activation – One aspect of macrophage cell biology that fascinates me is how macrophages migrate towards sites of infection and tissue damage. Macrophages can use a process called chemotaxis to sense where they are within concentration gradients of small proteins called chemokines.
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Publications
Selected recent papers:
- Biased agonists of GPR84 and insights into biological control. Luscombe, V. B., Wang, P., Russell, A. J., & Greaves, D. R. (2024). British Journal of Pharmacology, 181(10), 1509–1523. https://doi.org/10.1111/bph.16310
- Steric control of signaling bias in the immunometabolic receptor GPR84.Wang P, Zhang X, Guseinov AA, Jenkins L, von Hallerstein C, Colburn JD, Ives R, Luscombe VB, Marsango S, Oktavia L, Raja A, Greaves DR, Biggin PC, Milligan G, Zhang C, Tikhonova IG, Russell AJ.bioRxiv [Preprint]. 2025 Aug 2:2025.07.30.667614. doi: 10.1101/2025.07.30.667614.
- Kinetic insights into agonist-dependent signalling bias at the pro-inflammatory G-protein coupled receptor GPR84. Luscombe VB, Baena-López LA, Bataille CJR, Russell AJ, Greaves DR. Eur J Pharmacol. 2023 Aug 3;956:175960. doi: 10.1016/j.ejphar.2023.175960.
- Development of Highly Potent, G-Protein Pathway Biased, Selective, and Orally Bioavailable GPR84 Agonists. Wang P, Raja A, Luscombe VB, Bataille CJR, Lucy D, Rogga VV, Greaves DR, Russell AJ. J Med Chem. 2023 Dec 26;67(1):110-137. doi: 10.1021/acs.jmedchem.3c00951
- Drug repurposing in cardiovascular inflammation: Successes, failures, and future opportunities. Chaffey L, Roberti A, Greaves DR. Front Pharmacol. 2022 Oct 21;13:1046406. doi: 10.3389/fphar.2022.1046406.
- Cardiac lymphatics retain LYVE-1-dependent macrophages during neonatal mouse heart regeneration. Chapman BG, Klaourakis K, de Villiers C, Gunadasa-Rohling M, Cosma MA, Cooper STE, Mohan K, Weinberger M, Carr CA, Greaves DR, Jackson DG, Pezzolla D, Choudhury RP, Vieira JM, Riley PR. Nat Cardiovasc Res. 2025 Sep 17;4(10):1258-1276. doi: 10.1038/s44161-025-00711-4.
- Ly6Chi Monocytes Are Metabolically Reprogrammed in the Blood during Inflammatory Stimulation and Require Intact OxPhos for Chemotaxis and Monocyte to Macrophage Differentiation. Purvis GSD, McNeill E, Wright B, Channon KM, Greaves DR. Cells. 2024 May 26;13(11):916. doi: 10.3390/cells13110916.
- Bruton’s TK regulates myeloid cell recruitment during acute inflammation. Purvis GSD, Aranda-Tavio H, Channon KM, Greaves DR. Br J Pharmacol. 2022 Mar 15;179(11):2754-2770. doi: 10.1111/bph.15778.